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Gene Information

Gene symbol: CD44

Gene name: CD44 molecule (Indian blood group)

HGNC ID: 1681

Synonyms: IN, MC56, Pgp1, CD44R, HCELL, CSPG8

Related Genes

# Gene Symbol Number of hits
1 ACE 1 hits
2 ACTC1 1 hits
3 ACTN4 1 hits
4 AIM2 1 hits
5 AKT3 1 hits
6 AR 1 hits
7 B4GALT1 1 hits
8 B4GALT7 1 hits
9 CASP3 1 hits
10 CD226 1 hits
11 CD2AP 1 hits
12 CD59 1 hits
13 CD74 1 hits
14 CLDN1 1 hits
15 CLDN7 1 hits
16 COL1A1 1 hits
17 COL4A4 1 hits
18 CSPG4 1 hits
19 CTGF 1 hits
20 CXCL12 1 hits
21 CXCR4 1 hits
22 DDR1 1 hits
23 DPEP1 1 hits
24 EGF 1 hits
25 EPHB2 1 hits
26 ERBB2 1 hits
27 FGF4 1 hits
28 GALM 1 hits
29 GPC5 1 hits
30 HGF 1 hits
31 HK2 1 hits
32 HSPG2 1 hits
33 ICAM1 1 hits
34 IL8RB 1 hits
35 ILK 1 hits
36 ITGAV 1 hits
37 ITGB1 1 hits
38 KRT19 1 hits
39 MAPK3 1 hits
40 MIF 1 hits
41 MKI67 1 hits
42 NES 1 hits
43 NID1 1 hits
44 NOTCH3 1 hits
45 NPHS2 1 hits
46 PDGFB 1 hits
47 PDGFRA 1 hits
48 PTPRO 1 hits
49 ROBO4 1 hits
50 RORC 1 hits
51 SYNPO 1 hits
52 TJP1 1 hits
53 VCAM1 1 hits
54 VEGFA 1 hits
55 VIM 1 hits
56 WT1 1 hits

Related Sentences

# PMID Sentence
1 34740957 In patients with glomerulonephritis, AIM2 expression increased in CD44+-activated parietal epithelial cells within glomerular crescents.
2 34740957 In patients with glomerulonephritis, AIM2 expression increased in CD44+-activated parietal epithelial cells within glomerular crescents.
3 34740957 Aim2 -/- mice also demonstrated dysregulated cellular proliferation and an increase in CD44+ parietal epithelial cells during glomerulonephritis.
4 34740957 Aim2 -/- mice also demonstrated dysregulated cellular proliferation and an increase in CD44+ parietal epithelial cells during glomerulonephritis.
5 34740957 The AIM2-like receptor (ALR) locus was necessary for the inflammatory glomerulonephritis phenotype observed in Aim2 -/- mice, as NTS-treated ALR -/- mice displayed equal levels of injury as wild-type controls.
6 34740957 The AIM2-like receptor (ALR) locus was necessary for the inflammatory glomerulonephritis phenotype observed in Aim2 -/- mice, as NTS-treated ALR -/- mice displayed equal levels of injury as wild-type controls.
7 33641441 For immunostaining, parietal epithelial cells facing the injured glomeruli of BXSB/MpJ-Yaa expressed CD44, an activated parietal epithelial cell marker, and CD44-positive parietal epithelial cells showed nuclear localization of the androgen receptor and proliferation marker Ki67.
8 33641441 For immunostaining, parietal epithelial cells facing the injured glomeruli of BXSB/MpJ-Yaa expressed CD44, an activated parietal epithelial cell marker, and CD44-positive parietal epithelial cells showed nuclear localization of the androgen receptor and proliferation marker Ki67.
9 33641441 CD44- or Ki67-positive parietal epithelial cells were significantly fewer in castrated group than in sham-operated BXSB/MpJ-Yaa at six months.
10 33641441 CD44- or Ki67-positive parietal epithelial cells were significantly fewer in castrated group than in sham-operated BXSB/MpJ-Yaa at six months.
11 33544806 The proliferated parietal cells of Bowman's capsule proved to express cluster of differentiation 44 (CD44), whereas remnant podocytes and mesangial cells showed Wilms tumor 1 (WT1) positivity.
12 33544806 The proliferated parietal cells of Bowman's capsule proved to express cluster of differentiation 44 (CD44), whereas remnant podocytes and mesangial cells showed Wilms tumor 1 (WT1) positivity.
13 33544806 Since CD44 might be involved in fibrogenesis, but ACE inhibitors can exert a protective role against glomerular deterioration, we performed a synthesis of literature data which enabled us to propose a hypothesis with a potential clinical impact.
14 33544806 Since CD44 might be involved in fibrogenesis, but ACE inhibitors can exert a protective role against glomerular deterioration, we performed a synthesis of literature data which enabled us to propose a hypothesis with a potential clinical impact.
15 33544806 We conclude that, in patients with LVAD implants, high blood pressure and high serum level of angiotensin II, the association between ACE inhibitors and anti-CD44 agents might exert glomerular protection and increase the survival time.
16 33544806 We conclude that, in patients with LVAD implants, high blood pressure and high serum level of angiotensin II, the association between ACE inhibitors and anti-CD44 agents might exert glomerular protection and increase the survival time.
17 32628542 Previously, we showed that FFSS-induced upregulation of the cyclooxygenase 2 (COX2)-PGE2-prostaglandin E receptor 2 (EP2) axis in podocytes activates Akt-glycogen synthase kinase-3β-β-catenin and MAPK/ERK signaling in response to FFSS.
18 32628542 In the present study, we used previously characterized COX2 [prostaglandin-endoperoxide synthase 2 (Ptgs2)], EP2 (Ptger2), and β1-catenin (Ctnnb1) as "seed genes" from an array data set of four groups analyzed over a time course.
19 32628542 Further validation using Western blot analysis showed increased expression of phosho-Erbb2, phospho-mammalian target of rapamycin (mTOR), CD44, and hexokinase II (Hk2); decreased total Erbb2, galactose mutarotase (Galm), and β-1,4-galactosyltransferase 1 (B4galt1); and unchanged total mTOR and AKT3.
20 32597007 Vimentin and α-SMA, markers of changes to the epithelial cell phenotype, were present in PECs in aged CD44+/+ mice, but absent in aged CD44-/- mice in both outer cortical (OC) and juxtamedullary (JM) glomeruli.
21 32597007 Vimentin and α-SMA, markers of changes to the epithelial cell phenotype, were present in PECs in aged CD44+/+ mice, but absent in aged CD44-/- mice in both outer cortical (OC) and juxtamedullary (JM) glomeruli.
22 32597007 Vimentin and α-SMA, markers of changes to the epithelial cell phenotype, were present in PECs in aged CD44+/+ mice, but absent in aged CD44-/- mice in both outer cortical (OC) and juxtamedullary (JM) glomeruli.
23 32597007 Because age-related glomerular hypertrophy was lower in CD44-/- mice, mTOR activation was assessed by phospho-S6 ribosomal protein (pS6RP) staining.
24 32597007 Because age-related glomerular hypertrophy was lower in CD44-/- mice, mTOR activation was assessed by phospho-S6 ribosomal protein (pS6RP) staining.
25 32597007 Because age-related glomerular hypertrophy was lower in CD44-/- mice, mTOR activation was assessed by phospho-S6 ribosomal protein (pS6RP) staining.
26 32597007 These results show that the increase in CD44 in PECs in aged kidneys contributes to several changes to the glomerulus during healthy aging in mice, and may involve ERK and mTOR activation.
27 32597007 These results show that the increase in CD44 in PECs in aged kidneys contributes to several changes to the glomerulus during healthy aging in mice, and may involve ERK and mTOR activation.
28 32597007 These results show that the increase in CD44 in PECs in aged kidneys contributes to several changes to the glomerulus during healthy aging in mice, and may involve ERK and mTOR activation.
29 32068458 Biphasic MIF and SDF1 expression during podocyte injury promote CD44-mediated glomerular parietal cell migration in focal segmental glomerulosclerosis.
30 32068458 Biphasic MIF and SDF1 expression during podocyte injury promote CD44-mediated glomerular parietal cell migration in focal segmental glomerulosclerosis.
31 32068458 Biphasic MIF and SDF1 expression during podocyte injury promote CD44-mediated glomerular parietal cell migration in focal segmental glomerulosclerosis.
32 32068458 Biphasic MIF and SDF1 expression during podocyte injury promote CD44-mediated glomerular parietal cell migration in focal segmental glomerulosclerosis.
33 32068458 Biphasic MIF and SDF1 expression during podocyte injury promote CD44-mediated glomerular parietal cell migration in focal segmental glomerulosclerosis.
34 32068458 Biphasic MIF and SDF1 expression during podocyte injury promote CD44-mediated glomerular parietal cell migration in focal segmental glomerulosclerosis.
35 32068458 The present study focused on CD44 signaling, particularly the roles of two CD44-related chemokines, migration inhibitory factor (MIF) and stromal cell-derived factor 1 (SDF1), and their common receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), in the NEP25/LMB2 mouse podocyte-toxin model of FSGS.
36 32068458 The present study focused on CD44 signaling, particularly the roles of two CD44-related chemokines, migration inhibitory factor (MIF) and stromal cell-derived factor 1 (SDF1), and their common receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), in the NEP25/LMB2 mouse podocyte-toxin model of FSGS.
37 32068458 The present study focused on CD44 signaling, particularly the roles of two CD44-related chemokines, migration inhibitory factor (MIF) and stromal cell-derived factor 1 (SDF1), and their common receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), in the NEP25/LMB2 mouse podocyte-toxin model of FSGS.
38 32068458 The present study focused on CD44 signaling, particularly the roles of two CD44-related chemokines, migration inhibitory factor (MIF) and stromal cell-derived factor 1 (SDF1), and their common receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), in the NEP25/LMB2 mouse podocyte-toxin model of FSGS.
39 32068458 The present study focused on CD44 signaling, particularly the roles of two CD44-related chemokines, migration inhibitory factor (MIF) and stromal cell-derived factor 1 (SDF1), and their common receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), in the NEP25/LMB2 mouse podocyte-toxin model of FSGS.
40 32068458 The present study focused on CD44 signaling, particularly the roles of two CD44-related chemokines, migration inhibitory factor (MIF) and stromal cell-derived factor 1 (SDF1), and their common receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), in the NEP25/LMB2 mouse podocyte-toxin model of FSGS.
41 32068458 Expression of MIF and SDF1 was first increased in injured podocytes and subsequently transferred to activated PECs expressing CD44 and CXCR4.
42 32068458 Expression of MIF and SDF1 was first increased in injured podocytes and subsequently transferred to activated PECs expressing CD44 and CXCR4.
43 32068458 Expression of MIF and SDF1 was first increased in injured podocytes and subsequently transferred to activated PECs expressing CD44 and CXCR4.
44 32068458 Expression of MIF and SDF1 was first increased in injured podocytes and subsequently transferred to activated PECs expressing CD44 and CXCR4.
45 32068458 Expression of MIF and SDF1 was first increased in injured podocytes and subsequently transferred to activated PECs expressing CD44 and CXCR4.
46 32068458 Expression of MIF and SDF1 was first increased in injured podocytes and subsequently transferred to activated PECs expressing CD44 and CXCR4.
47 32068458 In an immortalized mouse PEC (mPEC) line, recombinant MIF and SDF1 (rMIF and rSDF1, respectively) individually increased CD44 and CXCR4 mRNA and protein levels. rMIF and rSDF1 stimulated endogenous MIF and SDF1 production. rMIF- and rSDF1-induced mPEC migration was suppressed by CD44 siRNA.
48 32068458 In an immortalized mouse PEC (mPEC) line, recombinant MIF and SDF1 (rMIF and rSDF1, respectively) individually increased CD44 and CXCR4 mRNA and protein levels. rMIF and rSDF1 stimulated endogenous MIF and SDF1 production. rMIF- and rSDF1-induced mPEC migration was suppressed by CD44 siRNA.
49 32068458 In an immortalized mouse PEC (mPEC) line, recombinant MIF and SDF1 (rMIF and rSDF1, respectively) individually increased CD44 and CXCR4 mRNA and protein levels. rMIF and rSDF1 stimulated endogenous MIF and SDF1 production. rMIF- and rSDF1-induced mPEC migration was suppressed by CD44 siRNA.
50 32068458 In an immortalized mouse PEC (mPEC) line, recombinant MIF and SDF1 (rMIF and rSDF1, respectively) individually increased CD44 and CXCR4 mRNA and protein levels. rMIF and rSDF1 stimulated endogenous MIF and SDF1 production. rMIF- and rSDF1-induced mPEC migration was suppressed by CD44 siRNA.
51 32068458 In an immortalized mouse PEC (mPEC) line, recombinant MIF and SDF1 (rMIF and rSDF1, respectively) individually increased CD44 and CXCR4 mRNA and protein levels. rMIF and rSDF1 stimulated endogenous MIF and SDF1 production. rMIF- and rSDF1-induced mPEC migration was suppressed by CD44 siRNA.
52 32068458 In an immortalized mouse PEC (mPEC) line, recombinant MIF and SDF1 (rMIF and rSDF1, respectively) individually increased CD44 and CXCR4 mRNA and protein levels. rMIF and rSDF1 stimulated endogenous MIF and SDF1 production. rMIF- and rSDF1-induced mPEC migration was suppressed by CD44 siRNA.
53 32068458 However, MIF and SDF1 inhibitors failed to show any impact on proteinuria, podocyte number, and CD44 expression in NEP25/LMB2 mice.
54 32068458 However, MIF and SDF1 inhibitors failed to show any impact on proteinuria, podocyte number, and CD44 expression in NEP25/LMB2 mice.
55 32068458 However, MIF and SDF1 inhibitors failed to show any impact on proteinuria, podocyte number, and CD44 expression in NEP25/LMB2 mice.
56 32068458 However, MIF and SDF1 inhibitors failed to show any impact on proteinuria, podocyte number, and CD44 expression in NEP25/LMB2 mice.
57 32068458 However, MIF and SDF1 inhibitors failed to show any impact on proteinuria, podocyte number, and CD44 expression in NEP25/LMB2 mice.
58 32068458 However, MIF and SDF1 inhibitors failed to show any impact on proteinuria, podocyte number, and CD44 expression in NEP25/LMB2 mice.
59 32068458 Our data suggest that injured podocytes upregulate MIF and SDF1 that stimulate CD44 expression and CD44-mediated migration, which is enhanced by endogenous MIF and SDF1 in PECs.
60 32068458 Our data suggest that injured podocytes upregulate MIF and SDF1 that stimulate CD44 expression and CD44-mediated migration, which is enhanced by endogenous MIF and SDF1 in PECs.
61 32068458 Our data suggest that injured podocytes upregulate MIF and SDF1 that stimulate CD44 expression and CD44-mediated migration, which is enhanced by endogenous MIF and SDF1 in PECs.
62 32068458 Our data suggest that injured podocytes upregulate MIF and SDF1 that stimulate CD44 expression and CD44-mediated migration, which is enhanced by endogenous MIF and SDF1 in PECs.
63 32068458 Our data suggest that injured podocytes upregulate MIF and SDF1 that stimulate CD44 expression and CD44-mediated migration, which is enhanced by endogenous MIF and SDF1 in PECs.
64 32068458 Our data suggest that injured podocytes upregulate MIF and SDF1 that stimulate CD44 expression and CD44-mediated migration, which is enhanced by endogenous MIF and SDF1 in PECs.
65 31630546 In healthy glomeruli, parietal epithelial cell (PEC)-derived extracellular matrix (ECM) proteins include laminin-β1, perlecan, and collagen type IV-α2 and podocyte-specific ECM proteins include laminin-β2, agrin, and collagen type IV-α4.
66 31630546 In healthy glomeruli, parietal epithelial cell (PEC)-derived extracellular matrix (ECM) proteins include laminin-β1, perlecan, and collagen type IV-α2 and podocyte-specific ECM proteins include laminin-β2, agrin, and collagen type IV-α4.
67 31630546 To determine the role of CD44, FSGS was induced in CD44-/- and CD44+/+ mice.
68 31630546 To determine the role of CD44, FSGS was induced in CD44-/- and CD44+/+ mice.
69 31630546 PEC staining for perlecan, collagen type IV-α2, laminin-β2, and agrin were significantly lower in diseased CD44-/- mice compared with diseased CD44+/+ mice.
70 31630546 PEC staining for perlecan, collagen type IV-α2, laminin-β2, and agrin were significantly lower in diseased CD44-/- mice compared with diseased CD44+/+ mice.
71 30285525 Focal and segmental glomerulosclerosis in murine models: a histological and ultrastructural characterization with immunohistochemistry correlation of glomerular CD44 and WT1 expression.
72 29673759 Like all basement membranes, the GBM contains type IV collagen, laminin, nidogen, and heparan sulfate proteoglycan.
73 29673759 Mutations that affect the GBM's collagen α3α4α5(IV) components cause Alport syndrome (kidney disease with variable ear and eye defects) and its variants, including thin basement membrane nephropathy.
74 29673759 The very different types of kidney diseases that result from mutations in collagen IV vs. laminin are likely due to very different pathogenic mechanisms.
75 27998643 Activated ERK1/2 increases CD44 in glomerular parietal epithelial cells leading to matrix expansion.
76 27998643 Activated ERK1/2 increases CD44 in glomerular parietal epithelial cells leading to matrix expansion.
77 27998643 Activated ERK1/2 increases CD44 in glomerular parietal epithelial cells leading to matrix expansion.
78 27998643 Activated ERK1/2 increases CD44 in glomerular parietal epithelial cells leading to matrix expansion.
79 27998643 Albuminuria, focal and global glomerulosclerosis (periodic acid-Schiff stain), and collagen IV staining were lower in CD44 knockout compared with wild-type mice with FSGS.
80 27998643 Albuminuria, focal and global glomerulosclerosis (periodic acid-Schiff stain), and collagen IV staining were lower in CD44 knockout compared with wild-type mice with FSGS.
81 27998643 Albuminuria, focal and global glomerulosclerosis (periodic acid-Schiff stain), and collagen IV staining were lower in CD44 knockout compared with wild-type mice with FSGS.
82 27998643 Albuminuria, focal and global glomerulosclerosis (periodic acid-Schiff stain), and collagen IV staining were lower in CD44 knockout compared with wild-type mice with FSGS.
83 27998643 In cultured murine parietal epithelial cells, overexpressing CD44 with a retroviral vector encoding CD44 was accompanied by significantly increased collagen IV expression and parietal epithelial cell migration.
84 27998643 In cultured murine parietal epithelial cells, overexpressing CD44 with a retroviral vector encoding CD44 was accompanied by significantly increased collagen IV expression and parietal epithelial cell migration.
85 27998643 In cultured murine parietal epithelial cells, overexpressing CD44 with a retroviral vector encoding CD44 was accompanied by significantly increased collagen IV expression and parietal epithelial cell migration.
86 27998643 In cultured murine parietal epithelial cells, overexpressing CD44 with a retroviral vector encoding CD44 was accompanied by significantly increased collagen IV expression and parietal epithelial cell migration.
87 27998643 Because our results showed de novo co-staining for activated ERK1/2 (pERK) in parietal epithelial cells in experimental FSGS, and also in biopsies from patients with FSGS, two in vitro strategies were employed to prove that pERK regulated CD44 levels.
88 27998643 Because our results showed de novo co-staining for activated ERK1/2 (pERK) in parietal epithelial cells in experimental FSGS, and also in biopsies from patients with FSGS, two in vitro strategies were employed to prove that pERK regulated CD44 levels.
89 27998643 Because our results showed de novo co-staining for activated ERK1/2 (pERK) in parietal epithelial cells in experimental FSGS, and also in biopsies from patients with FSGS, two in vitro strategies were employed to prove that pERK regulated CD44 levels.
90 27998643 Because our results showed de novo co-staining for activated ERK1/2 (pERK) in parietal epithelial cells in experimental FSGS, and also in biopsies from patients with FSGS, two in vitro strategies were employed to prove that pERK regulated CD44 levels.
91 27440779 Additionally, markers of epithelial-to-mesenchymal transition (platelet-derived growth factor receptor-β, α-smooth muscle actin, Notch-3) and PEC activation (CD44, collagen IV) were further increased by mTOR reduction.
92 26453615 Macrophage Migration Inhibitory Factor Mediates Proliferative GN via CD74.
93 26453615 Macrophage Migration Inhibitory Factor Mediates Proliferative GN via CD74.
94 26453615 Macrophage Migration Inhibitory Factor Mediates Proliferative GN via CD74.
95 26453615 Macrophage Migration Inhibitory Factor Mediates Proliferative GN via CD74.
96 26453615 Macrophage Migration Inhibitory Factor Mediates Proliferative GN via CD74.
97 26453615 Macrophage Migration Inhibitory Factor Mediates Proliferative GN via CD74.
98 26453615 Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that mediates inflammation by engagement of a receptor complex involving the components CD74, CD44, CXCR2, and CXCR4.
99 26453615 Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that mediates inflammation by engagement of a receptor complex involving the components CD74, CD44, CXCR2, and CXCR4.
100 26453615 Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that mediates inflammation by engagement of a receptor complex involving the components CD74, CD44, CXCR2, and CXCR4.
101 26453615 Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that mediates inflammation by engagement of a receptor complex involving the components CD74, CD44, CXCR2, and CXCR4.
102 26453615 Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that mediates inflammation by engagement of a receptor complex involving the components CD74, CD44, CXCR2, and CXCR4.
103 26453615 Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that mediates inflammation by engagement of a receptor complex involving the components CD74, CD44, CXCR2, and CXCR4.
104 26453615 The proliferative effects of MIF may involve CD74 together with the coreceptor and PEC activation marker CD44.
105 26453615 The proliferative effects of MIF may involve CD74 together with the coreceptor and PEC activation marker CD44.
106 26453615 The proliferative effects of MIF may involve CD74 together with the coreceptor and PEC activation marker CD44.
107 26453615 The proliferative effects of MIF may involve CD74 together with the coreceptor and PEC activation marker CD44.
108 26453615 The proliferative effects of MIF may involve CD74 together with the coreceptor and PEC activation marker CD44.
109 26453615 The proliferative effects of MIF may involve CD74 together with the coreceptor and PEC activation marker CD44.
110 26453615 Herein, we analyzed the effects of local glomerular MIF/CD74/CD44 signaling in proliferative glomerulonephritides.
111 26453615 Herein, we analyzed the effects of local glomerular MIF/CD74/CD44 signaling in proliferative glomerulonephritides.
112 26453615 Herein, we analyzed the effects of local glomerular MIF/CD74/CD44 signaling in proliferative glomerulonephritides.
113 26453615 Herein, we analyzed the effects of local glomerular MIF/CD74/CD44 signaling in proliferative glomerulonephritides.
114 26453615 Herein, we analyzed the effects of local glomerular MIF/CD74/CD44 signaling in proliferative glomerulonephritides.
115 26453615 Herein, we analyzed the effects of local glomerular MIF/CD74/CD44 signaling in proliferative glomerulonephritides.
116 26453615 MIF, CD74, and CD44 were upregulated in the glomeruli of patients and mice with proliferative glomerulonephritides.
117 26453615 MIF, CD74, and CD44 were upregulated in the glomeruli of patients and mice with proliferative glomerulonephritides.
118 26453615 MIF, CD74, and CD44 were upregulated in the glomeruli of patients and mice with proliferative glomerulonephritides.
119 26453615 MIF, CD74, and CD44 were upregulated in the glomeruli of patients and mice with proliferative glomerulonephritides.
120 26453615 MIF, CD74, and CD44 were upregulated in the glomeruli of patients and mice with proliferative glomerulonephritides.
121 26453615 MIF, CD74, and CD44 were upregulated in the glomeruli of patients and mice with proliferative glomerulonephritides.
122 26453615 During disease, CD74 and CD44 were expressed de novo in PECs and colocalized in both PECs and mesangial cells.
123 26453615 During disease, CD74 and CD44 were expressed de novo in PECs and colocalized in both PECs and mesangial cells.
124 26453615 During disease, CD74 and CD44 were expressed de novo in PECs and colocalized in both PECs and mesangial cells.
125 26453615 During disease, CD74 and CD44 were expressed de novo in PECs and colocalized in both PECs and mesangial cells.
126 26453615 During disease, CD74 and CD44 were expressed de novo in PECs and colocalized in both PECs and mesangial cells.
127 26453615 During disease, CD74 and CD44 were expressed de novo in PECs and colocalized in both PECs and mesangial cells.
128 26453615 Stress stimuli induced MIF secretion from glomerular cells in vitro and in vivo, in particular from podocytes, and MIF stimulation induced proliferation of PECs and mesangial cells via CD74.
129 26453615 Stress stimuli induced MIF secretion from glomerular cells in vitro and in vivo, in particular from podocytes, and MIF stimulation induced proliferation of PECs and mesangial cells via CD74.
130 26453615 Stress stimuli induced MIF secretion from glomerular cells in vitro and in vivo, in particular from podocytes, and MIF stimulation induced proliferation of PECs and mesangial cells via CD74.
131 26453615 Stress stimuli induced MIF secretion from glomerular cells in vitro and in vivo, in particular from podocytes, and MIF stimulation induced proliferation of PECs and mesangial cells via CD74.
132 26453615 Stress stimuli induced MIF secretion from glomerular cells in vitro and in vivo, in particular from podocytes, and MIF stimulation induced proliferation of PECs and mesangial cells via CD74.
133 26453615 Stress stimuli induced MIF secretion from glomerular cells in vitro and in vivo, in particular from podocytes, and MIF stimulation induced proliferation of PECs and mesangial cells via CD74.
134 26453615 Our data suggest a novel molecular mechanism and glomerular cell crosstalk by which local upregulation of MIF and its receptor complex CD74/CD44 mediate glomerular injury and pathologic proliferation in GN.
135 26453615 Our data suggest a novel molecular mechanism and glomerular cell crosstalk by which local upregulation of MIF and its receptor complex CD74/CD44 mediate glomerular injury and pathologic proliferation in GN.
136 26453615 Our data suggest a novel molecular mechanism and glomerular cell crosstalk by which local upregulation of MIF and its receptor complex CD74/CD44 mediate glomerular injury and pathologic proliferation in GN.
137 26453615 Our data suggest a novel molecular mechanism and glomerular cell crosstalk by which local upregulation of MIF and its receptor complex CD74/CD44 mediate glomerular injury and pathologic proliferation in GN.
138 26453615 Our data suggest a novel molecular mechanism and glomerular cell crosstalk by which local upregulation of MIF and its receptor complex CD74/CD44 mediate glomerular injury and pathologic proliferation in GN.
139 26453615 Our data suggest a novel molecular mechanism and glomerular cell crosstalk by which local upregulation of MIF and its receptor complex CD74/CD44 mediate glomerular injury and pathologic proliferation in GN.
140 26403399 In addition, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF) and cluster of differentiation (CD) 44 were observed by Masson staining and detected with immunohistochemistry (IHC) to confirm homing and location of mesenchymal stem cells (MSCs).
141 26403399 Moreover, Western Blot was used for detecting VEGF and CTGF so as to explore the possible mechanism of applying UMSC in treating IgAN.
142 26403399 MSCs were observed to be located in glomerulus and renal interstitium by IHC detection of CD44 and IHC qualitative observation of VEGF and CTGF had different positive expressions in three groups.
143 26403399 Furthermore, different expressions of VEGF and CTGF were observed quantitatively by Western Blot.
144 26260163 Hereditary angiopathy, nephropathy, aneurysms, and muscle cramps (HANAC) syndrome is an autosomal dominant syndrome caused by mutations in COL4A1 that encodes the α1 chain of collagen IV, a major component of basement membranes.
145 26260163 Abnormal structure of Bowman's capsule was associated with metalloproteinase induction and activation of the glomerular parietal epithelial cells that abnormally expressed CD44,α-SMA, ILK, and DDR1.
146 26260163 These results reveal a developmental role for the α1α1α2 collagen IV molecule in the embryonic glomerular basement membrane, affecting podocyte differentiation.
147 26017974 In addition to segmental and global glomerulosclerosis in older mice, staining for matrix proteins collagen type IV and heparan sulfate proteoglycan were markedly increased in Bowman's capsules of older mouse glomeruli, consistent with increased extracellular matrix production by PECs.
148 26017974 The mural cell markers neural/glial antigen 2, PDGF receptor-β, and CD146 as well as Notch 3 were also substantially increased in aged PECs.
149 25987249 We recently identified the gene for glypican-5 (GPC5), a cell-surface heparan sulfate proteoglycan, as conferring susceptibility for acquired nephrotic syndrome and additionally identified an association through a genome-wide association study between a variant in GPC5 and DN of type 2 diabetes mellitus.
150 25987249 In this study, diabetic kidney showed that accumulation of fibroblast growth factor (Fgf)2 strikingly induced progressive proteinuria that was avoided in Gpc5 knockdown mice.
151 25987249 Extraglomerular Fgf2 was pathogenic in DN, and the deterrence of Gpc5 effectively inhibited the glomerular accumulation of Fgf2, the subsequent increase of mesangial extracellular matrix, and the podocytes' small GTPase activity.
152 25853334 For each biopsy, one section was quadruple stained for PECs (ANXA3), podocytes (synaptopodin), PEC matrix (LKIV69), and Hoechst (nuclei), and a second was quadruple stained for activated PECs (CD44 and cytokeratin-19), PEC matrix, and nuclei.
153 25736496 These isolated Nestin(+) cells expressed the typical cell-surface marker of MSC, including Sca-1, CD44, CD106, NG2 and PDGFR-α.
154 25307344 Ninety-five renal biopsies were stained for claudin-1 (PEC marker), CD44 (activated PECs), and LKIV69 (PEC matrix); 38 had been diagnosed as early primary FSGS and 57 as minimal change disease.
155 25307344 Two novel PEC markers A-kinase anchor protein 12 and annexin A3 exhibited similar sensitivity.
156 24790760 CD59, CD44, IBP7, Robo4, and DPEP1 were the most significant differentially expressed proteins.
157 23826724 CD44 is a transmembrane adhesion glycoprotein, functioning as a hyaluronan receptor and participating in the uptake and degradation of hyaluronan.
158 21519194 The main components of the GBM are laminin-521 (α5β2γ1), collagen α3α4α5(IV), nidogen and the heparan sulfate proteoglycan, agrin.
159 21519194 In contrast, mutations that affect GBM collagen IV or agrin do not impair glomerular development or cause immediate leakage of plasma proteins.
160 21519194 However, collagen IV mutation, which causes Alport syndrome and ESRD in humans, leads to gradual damage to the GBM that eventually leads to albuminuria and renal failure.
161 20031026 This study demonstrates that the expression of the mesenchymal markers CD29 and CD44, the epithelial markers CD51 and ZO-1 and the podocyte markers CD2AP and NPHS2 can be induced in these cells via incubation with epidermal growth factor/platelet-derived growth factor BB and fibroblast growth factor 4/hepatocyte growth factor, respectively.
162 15258770 ICAM-1 and CD44, the ligation of which induces migratory behaviors, were absent from healthy podocytes but expressed by some podocytes in glomerulonephritis.
163 10500175 The mRNA expression of glomerular epithelial protein 1 (a marker for renal podocytes), anti-heparan-sulfate-proteoglycan antibody reactivity, and wheat germ agglutinin lectin staining of the metanephros were unaffected.
164 6235751 Localization of collagen types IV and V, laminin, and heparan sulfate proteoglycan to the basal lamina of kidney epithelial cells in transfilter metanephric culture.