Ignet

Gene Information

Gene symbol: TJP1

Gene name: tight junction protein 1

HGNC ID: 11827

Synonyms: ZO-1, MGC133289, DKFZp686M05161

Related Genes

#	Gene Symbol	Number of hits
1	ACTN4	1 hits
2	ADCYAP1	1 hits
3	ADIPOQ	1 hits
4	AGT	1 hits
5	AKT1	1 hits
6	ALB	1 hits
7	AMICA1	1 hits
8	CCL2	1 hits
9	CDH3	1 hits
10	CGN	1 hits
11	CLDN1	1 hits
12	CLDN5	1 hits
13	CLDN7	1 hits
14	CTNNB1	1 hits
15	CYBB	1 hits
16	DES	1 hits
17	F11R	1 hits
18	FOXP3	1 hits
19	GCG	1 hits
20	GJA1	1 hits
21	GPSN2	1 hits
22	HIF1A	1 hits
23	ICAM1	1 hits
24	IGF1	1 hits
25	IL1B	1 hits
26	INS	1 hits
27	JUP	1 hits
28	KIRREL	1 hits
29	MARVELD2	1 hits
30	MLLT4	1 hits
31	NOX5	1 hits
32	NPHS1	1 hits
33	OCLN	1 hits
34	PRKAA2	1 hits
35	PRKCA	1 hits
36	S100A4	1 hits
37	SETD2	1 hits
38	SOD1	1 hits
39	TGFB1	1 hits
40	TJP2	1 hits
41	TJP3	1 hits
42	VEGFA	1 hits
43	VIP	1 hits

Related Sentences

#	PMID	Sentence
1	10758223	The mechanism of breakdown of the blood retinal barriers is likely to be changes to the tight junction proteins including occludin and ZO-1.
2	11958524	Diabetes-related changes in rat cerebral occludin and zonula occludens-1 (ZO-1) expression.
3	11958524	To test this hypothesis, Western and Northern blot analysis were carried out to measure the steady-state level of occludin and zonula occludens-one (ZO-1) proteins and mRNA levels in cerebral tissue of streptozotocin-induced diabetic rats and the results were compared to insulin treated diabetic rats and vehicle injected control rats.
4	11958524	The cerebral occludin content in diabetic rats (115.4 +/- 18.6 arbitrary units) was significantly reduced compared to insulin-treated diabetic rats (649.1 +/- 141.2) or control rats (552.9 +/- 82.9), p < 0.001.
5	11958524	Diabetes-related changes in rat cerebral occludin and zonula occludens-1 (ZO-1) expression.
6	11958524	To test this hypothesis, Western and Northern blot analysis were carried out to measure the steady-state level of occludin and zonula occludens-one (ZO-1) proteins and mRNA levels in cerebral tissue of streptozotocin-induced diabetic rats and the results were compared to insulin treated diabetic rats and vehicle injected control rats.
7	11958524	The cerebral occludin content in diabetic rats (115.4 +/- 18.6 arbitrary units) was significantly reduced compared to insulin-treated diabetic rats (649.1 +/- 141.2) or control rats (552.9 +/- 82.9), p < 0.001.
8	12535867	Because the cerebral microcirculation is much less affected in diabetes, our objectives are to compare: (1) glutathione peroxidase activity, (2) superoxide dismutase levels, (3) superoxide production, and (4) junctional protein (ZO-1) levels between retinal and brain-derived endothelial cells.
9	12535867	The results demonstrate that, compared to brain-derived endothelial cells, retinal endothelial cells release high levels of superoxide, have less glutathione peroxidase activity and lower levels of superoxide dismutase, and ZO-1.
10	12535867	Because the cerebral microcirculation is much less affected in diabetes, our objectives are to compare: (1) glutathione peroxidase activity, (2) superoxide dismutase levels, (3) superoxide production, and (4) junctional protein (ZO-1) levels between retinal and brain-derived endothelial cells.
11	12535867	The results demonstrate that, compared to brain-derived endothelial cells, retinal endothelial cells release high levels of superoxide, have less glutathione peroxidase activity and lower levels of superoxide dismutase, and ZO-1.
12	12633933	Age-related changes in rat cerebral occludin and zonula occludens-1 (ZO-1).
13	12633933	To test this hypothesis, Western and Northern blot analysis were carried out to measure the steady-state level of occludin and zonula occludens-one (ZO-1) proteins and their mRNA in cerebral tissue of 3-, 12- and 24-month-old rats.
14	12633933	Age-related changes in rat cerebral occludin and zonula occludens-1 (ZO-1).
15	12633933	To test this hypothesis, Western and Northern blot analysis were carried out to measure the steady-state level of occludin and zonula occludens-one (ZO-1) proteins and their mRNA in cerebral tissue of 3-, 12- and 24-month-old rats.
16	15063759	Mice lacking insulin or insulin-like growth factor 1 receptors in vascular endothelial cells maintain normal blood-brain barrier.
17	15063759	One of the key tight junction proteins, zona occludens-1 (ZO-1), has been reported to be stimulated in its expression by insulin and IGF-1.
18	15063759	To assess the role of insulin and IGF-1 in endothelial cells in the BBB we have utilized mice with a vascular endothelial cell-specific knockout of the insulin receptor (VENIRKO) and IGF-1 receptor (VENIFARKO).
19	15063759	These observations indicate that neither insulin nor IGF-1 signaling in vascular endothelial cells is required for development and maintenance of BBB or BRB.
20	15109567	The goal of this review was to elucidate potential mechanisms by which elevated growth factors elicit deregulated paracellular permeability via altered regulation of tight junctions, with particular emphasis on the tight junction proteins occludin and ZO-1, protein kinase C signaling, and endocytosis of junctional proteins.
21	16567508	Exposure of rat glomerular epithelial cells to high glucose resulted in a decrease in the intensity of ZO-1 staining and redistribution of ZO-1 from the membrane to the cytoplasm, changes that are attenuated by blockade of the angiotensin II type 1 receptor.
22	16724250	The localization of the following tight junction (TJ)-associated proteins was studied: occludin as an integral membrane (transmembrane) protein, and zonula occludens one (ZO-1) as a peripheral protein.
23	16724250	The localization of beta-catenin as a representative of the cadherin/catenin complex that is typical for adherens junctions (AJs) also was studied.
24	16724250	No significant differences in the density of immunosignals for ZO-1 and beta-catenin between both experimental mouse groups were observed.
25	16724250	The localization of the following tight junction (TJ)-associated proteins was studied: occludin as an integral membrane (transmembrane) protein, and zonula occludens one (ZO-1) as a peripheral protein.
26	16724250	The localization of beta-catenin as a representative of the cadherin/catenin complex that is typical for adherens junctions (AJs) also was studied.
27	16724250	No significant differences in the density of immunosignals for ZO-1 and beta-catenin between both experimental mouse groups were observed.
28	18431508	In cultured podocytes, adiponectin administration was associated with increased activity of AMPK, and both adiponectin and AMPK activation reduced podocyte permeability to albumin and podocyte dysfunction, as evidenced by zona occludens-1 translocation to the membrane.
29	18431508	These effects seemed to be caused by reduction of oxidative stress, as adiponectin and AMPK activation both reduced protein levels of the NADPH oxidase Nox4 in podocytes.
30	18431508	Ad(-/-) mice treated with adiponectin exhibited normalization of albuminuria, improvement of podocyte foot process effacement, increased glomerular AMPK activation, and reduced urinary and glomerular markers of oxidant stress.
31	18431508	These results suggest that adiponectin is a key regulator of albuminuria, likely acting through the AMPK pathway to modulate oxidant stress in podocytes.
32	18838678	Combination therapy with AT1 blocker and vitamin D analog markedly ameliorates diabetic nephropathy: blockade of compensatory renin increase.
33	18838678	Here we demonstrated that combination therapy with an AT1 receptor blocker and a vitamin D analog markedly ameliorated renal injury in the streptozotocin (STZ)-induced diabetes model due to the blockade of the compensatory renin rise by the vitamin D analog, leading to more effective RAS inhibition.
34	18838678	STZ-treated diabetic DBA/2J mice developed progressive albuminuria and glomerulosclerosis within 13 weeks, accompanied by increased intrarenal production of angiotensin (Ang) II, fibronection, TGF-beta, and MCP-1 and decreased expression of slit diaphragm proteins.
35	18838678	The combined treatment suppressed the induction of fibronection, TGF-beta, and MCP-1 and reversed the decline of slit diaphragm proteins nephrin, Neph-1, ZO-1, and alpha-actinin-4.
36	18838678	These were accompanied by blockade of intrarenal renin and Ang II accumulation induced by hyperglycemia and losartan.
37	19103180	In both cases there were typical signs of disruption of the BBB manifested by the absence of tight junction proteins (occludin, claudin-5, ZO-1 and JAM-1) in the parenchymal blood vessels, as well as albumin extravasation in examined brain areas.
38	19103180	The neuroinflammatory markers chemokine CCL2, NF-kappaB and nitrotyrosine were localized in the perivascular areas of the disrupted BBB and diffusely distributed in the brain parenchyma.
39	19963272	AGE-BSA also increased the PREC permeability by stimulating the expression of intracellular adhesion molecule-1 (ICAM-1) and decreased the expression of occludin and ZO-1.
40	19963272	Further, Ag-NPs inhibited the AGE-BSA-induced permeability by increased expression of tight junction proteins occludin and ZO-1, co-incident with an increase in barrier properties of endothelial monolayer.
41	19963272	AGE-BSA also increased the PREC permeability by stimulating the expression of intracellular adhesion molecule-1 (ICAM-1) and decreased the expression of occludin and ZO-1.
42	19963272	Further, Ag-NPs inhibited the AGE-BSA-induced permeability by increased expression of tight junction proteins occludin and ZO-1, co-incident with an increase in barrier properties of endothelial monolayer.
43	20110406	Increased vascular permeability of diabetic retina was accompanied by a decrease of zonula occludens (ZO)-1 and ZO-2 expression.
44	20110406	In diabetic retina and advanced glycation end product-treated human retinal microvascular endothelial cells, vascular leakage and loss of ZO-1 and ZO-2 on retinal vessels were effectively restored or prevented with treatment of rottlerin, transfection of PKC-delta-DN, or siRNA for PKC delta.
45	20110406	Increased vascular permeability of diabetic retina was accompanied by a decrease of zonula occludens (ZO)-1 and ZO-2 expression.
46	20110406	In diabetic retina and advanced glycation end product-treated human retinal microvascular endothelial cells, vascular leakage and loss of ZO-1 and ZO-2 on retinal vessels were effectively restored or prevented with treatment of rottlerin, transfection of PKC-delta-DN, or siRNA for PKC delta.
47	21228103	An increase in the renal levels of VEGF-A, VEGFR-2, transforming growth factor (TGF)-β1, and monocyte chemoattractant protein-1 in diabetic animals was significantly suppressed by AdhVASH-1 (immunoblotting).
48	21228103	AdhVASH-1 treatment significantly recovered the loss and altered the distribution patterns of nephrin and zonula occludens (ZO)-1 and suppressed the increase in the number of fibroblast-specific protein-1 (FSP-1(+)) and desmin(+) podocytes in diabetic mice.
49	21228103	In vitro, recombinant human VASH-1 (rhVASH-1) dose dependently suppressed the upregulation of VEGF induced by high ambient glucose (25 mM) in cultured mouse podocytes.
50	21228103	In addition, rhVASH-1 significantly recovered the mRNA levels of nephrin and the protein levels of ZO-1 and P-cadherin and suppressed the increase in protein levels of desmin, FSP-1, Snail, and Slug in podocytes under high-glucose condition.
51	21228103	An increase in the renal levels of VEGF-A, VEGFR-2, transforming growth factor (TGF)-β1, and monocyte chemoattractant protein-1 in diabetic animals was significantly suppressed by AdhVASH-1 (immunoblotting).
52	21228103	AdhVASH-1 treatment significantly recovered the loss and altered the distribution patterns of nephrin and zonula occludens (ZO)-1 and suppressed the increase in the number of fibroblast-specific protein-1 (FSP-1(+)) and desmin(+) podocytes in diabetic mice.
53	21228103	In vitro, recombinant human VASH-1 (rhVASH-1) dose dependently suppressed the upregulation of VEGF induced by high ambient glucose (25 mM) in cultured mouse podocytes.
54	21228103	In addition, rhVASH-1 significantly recovered the mRNA levels of nephrin and the protein levels of ZO-1 and P-cadherin and suppressed the increase in protein levels of desmin, FSP-1, Snail, and Slug in podocytes under high-glucose condition.
55	21617913	HIF-1 is involved in high glucose-induced paracellular permeability of brain endothelial cells.
56	21617913	Here we investigated the role of hypoxia-inducible factor-1 (HIF-1) in high glucose-induced endothelial permeability in vitro using mouse brain microvascular endothelial cells (b.End3).
57	21617913	Our results demonstrated that high glucose (30 mM) upregulated the protein level of HIF-1α, the regulatable subunit of HIF-1, and increased the transcriptional activity of HIF-1 in the endothelial cells.
58	21617913	At the same time, high glucose increased the paracellular permeability associated with diminished expression and disrupted continuity of tight junction proteins occludin and zona occludens protein-1 (ZO-1) of the endothelial cells.
59	21617913	Upregulating HIF-1 activity by cobalt chloride increased the paracellular permeability of the endothelial cells exposed to normal glucose (5.5 mM).
60	21617913	In contrast, downregulating HIF-1 activity by HIF-1α inhibitors and HIF-1α specific siRNA ameliorated the increased paracellular permeability and the alterations of distribution pattern of occludin and ZO-1 induced by high glucose.
61	21617913	In addition, high glucose increased expression of vascular endothelial growth factor (VEGF), a downstream gene of HIF-1.
62	21617913	Inhibiting VEGF improved the expression pattern of occludin and ZO-1, and attenuated the endothelial leakage.
63	21617913	These results strongly indicate that HIF-1 plays an important role in high glucose-induced BBB dysfunction.
64	21617913	HIF-1 is involved in high glucose-induced paracellular permeability of brain endothelial cells.
65	21617913	Here we investigated the role of hypoxia-inducible factor-1 (HIF-1) in high glucose-induced endothelial permeability in vitro using mouse brain microvascular endothelial cells (b.End3).
66	21617913	Our results demonstrated that high glucose (30 mM) upregulated the protein level of HIF-1α, the regulatable subunit of HIF-1, and increased the transcriptional activity of HIF-1 in the endothelial cells.
67	21617913	At the same time, high glucose increased the paracellular permeability associated with diminished expression and disrupted continuity of tight junction proteins occludin and zona occludens protein-1 (ZO-1) of the endothelial cells.
68	21617913	Upregulating HIF-1 activity by cobalt chloride increased the paracellular permeability of the endothelial cells exposed to normal glucose (5.5 mM).
69	21617913	In contrast, downregulating HIF-1 activity by HIF-1α inhibitors and HIF-1α specific siRNA ameliorated the increased paracellular permeability and the alterations of distribution pattern of occludin and ZO-1 induced by high glucose.
70	21617913	In addition, high glucose increased expression of vascular endothelial growth factor (VEGF), a downstream gene of HIF-1.
71	21617913	Inhibiting VEGF improved the expression pattern of occludin and ZO-1, and attenuated the endothelial leakage.
72	21617913	These results strongly indicate that HIF-1 plays an important role in high glucose-induced BBB dysfunction.
73	21617913	HIF-1 is involved in high glucose-induced paracellular permeability of brain endothelial cells.
74	21617913	Here we investigated the role of hypoxia-inducible factor-1 (HIF-1) in high glucose-induced endothelial permeability in vitro using mouse brain microvascular endothelial cells (b.End3).
75	21617913	Our results demonstrated that high glucose (30 mM) upregulated the protein level of HIF-1α, the regulatable subunit of HIF-1, and increased the transcriptional activity of HIF-1 in the endothelial cells.
76	21617913	At the same time, high glucose increased the paracellular permeability associated with diminished expression and disrupted continuity of tight junction proteins occludin and zona occludens protein-1 (ZO-1) of the endothelial cells.
77	21617913	Upregulating HIF-1 activity by cobalt chloride increased the paracellular permeability of the endothelial cells exposed to normal glucose (5.5 mM).
78	21617913	In contrast, downregulating HIF-1 activity by HIF-1α inhibitors and HIF-1α specific siRNA ameliorated the increased paracellular permeability and the alterations of distribution pattern of occludin and ZO-1 induced by high glucose.
79	21617913	In addition, high glucose increased expression of vascular endothelial growth factor (VEGF), a downstream gene of HIF-1.
80	21617913	Inhibiting VEGF improved the expression pattern of occludin and ZO-1, and attenuated the endothelial leakage.
81	21617913	These results strongly indicate that HIF-1 plays an important role in high glucose-induced BBB dysfunction.
82	21715347	While the expression of adherens junction protein β-catenin, and tight junction proteins occludin and ZO-1 was unchanged, the formation of these junctions after wound closure was delayed.
83	21832836	Lower expression of tight junction protein 1 gene and increased FOXP3 expression in the small bowel mucosa in coeliac disease and associated type 1 diabetes mellitus.
84	21874452	In addition, methods for assessing mRNA expression and protein content of the main TJ proteins (occludin, zonula occludens-1 [ZO-1]) are detailed.
85	22022184	In confocal imaging, ZO-1 colocalized with actin filaments and β-catenin at cell contact areas, forming intercellular filtration gaps.
86	22184542	This review first examines the major macromolecular components of the TJs (occludin, claudins, junctional adhesion molecule and tricellulin) and then the associated macromolecules at the intracellular plaque [zonula occludens (ZO)-1, ZO-2, ZO-3, AF-6, cingulin, 7H6].
87	22455314	In fibroblasts from the human chronic DFU wound edge there was a striking and significant 10-fold elevation of Cx43 protein, as well as a 6-fold increase in N-cadherin and a 2-fold increase in ZO-1 (zonular occludin-1), compared with unwounded skin.
88	23019073	Pigment epithelium-derived factor (PEDF) peptide eye drops reduce inflammation, cell death and vascular leakage in diabetic retinopathy in Ins2(Akita) mice.
89	23019073	Here, we evaluated intraocular deliverability features of two pigment epithelium-derived factor (PEDF) derivatives given as eye drops and their efficacy in modulating diabetes-induced retinal complications.
90	23019073	The antiangiogenic PEDF60-77 (P60) and neuroprotective PEDF78-121 (P78) derivatives were applied to Ins2(Akita) mouse eyes once a week for 15 wks at the onset of hyperglycemia.
91	23019073	Peak vitreous levels were 0.2 μg/mL for P60 and 0.9 μg/mL for P78 after 0.5 and 4 h, respectively.
92	23019073	Both peptides reduced vascular leakage by ~60% and increased zona occludens 1 (ZO1) and occludin expression in the microvasculature to nondiabetic levels.
93	23019073	P60 induced pERK1/2 and P78 promoted pAKT in Muller glia, two signals that were dampened in diabetic conditions.
94	23019073	Pharmacologically inhibiting AKT signaling in the retina blocked effects of the peptides on ZO1 and occludin expression.
95	23019073	P78 reduced levels of 9/20 cytokines in diabetic vitreous including interferon (IFN)-γ, interleukin (IL)-6, IL-3 and tumor necrosis factor (TNF)-α.
96	23019073	P60 lowered levels of 6/20 cytokines but was less effective than P78.
97	23019073	Pigment epithelium-derived factor (PEDF) peptide eye drops reduce inflammation, cell death and vascular leakage in diabetic retinopathy in Ins2(Akita) mice.
98	23019073	Here, we evaluated intraocular deliverability features of two pigment epithelium-derived factor (PEDF) derivatives given as eye drops and their efficacy in modulating diabetes-induced retinal complications.
99	23019073	The antiangiogenic PEDF60-77 (P60) and neuroprotective PEDF78-121 (P78) derivatives were applied to Ins2(Akita) mouse eyes once a week for 15 wks at the onset of hyperglycemia.
100	23019073	Peak vitreous levels were 0.2 μg/mL for P60 and 0.9 μg/mL for P78 after 0.5 and 4 h, respectively.
101	23019073	Both peptides reduced vascular leakage by ~60% and increased zona occludens 1 (ZO1) and occludin expression in the microvasculature to nondiabetic levels.
102	23019073	P60 induced pERK1/2 and P78 promoted pAKT in Muller glia, two signals that were dampened in diabetic conditions.
103	23019073	Pharmacologically inhibiting AKT signaling in the retina blocked effects of the peptides on ZO1 and occludin expression.
104	23019073	P78 reduced levels of 9/20 cytokines in diabetic vitreous including interferon (IFN)-γ, interleukin (IL)-6, IL-3 and tumor necrosis factor (TNF)-α.
105	23019073	P60 lowered levels of 6/20 cytokines but was less effective than P78.
106	23108103	Occludin glycation and ZO-1 disruption were prevented by N-acetylcysteine (NAC).
107	23220033	Ameliorative effect of PACAP and VIP against increased permeability in a model of outer blood retinal barrier dysfunction.
108	23220033	Previously it has been shown that PACAP and VIP are protective against several types of retinal injuries.
109	23220033	Here, using an in vitro model of DME, we explored the effects of both PACAP and VIP.
110	23220033	Effects of PACAP or VIP on cells permeability were evaluated by measuring both apical-to-basolateral movements of fluorescein isothyocyanate (FITC) dextran and transepithelial electrical resistance (TEER).
111	23220033	PACAP or VIP reversed both of these effects.
112	23220033	Furthermore, HG+IL-1β-induced reduction of claudin-1 and ZO-1 expression was reversed by PACAP and VIP.
113	23284911	The ECM degrading enzyme, heparanase, is secreted by cells as pro-heparanase that is internalized through low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1) to become enzymatically active.
114	23284911	Both apoE and pro-heparanase bind the LRP-1.
115	23284911	We further hypothesized that an apoE mimetic peptide (apoEdp) would inhibit the production of active heparanase by blocking LRP-1-mediated uptake of pro-heparanase and thereby decrease degradation of the ECM.
116	23284911	Treatment of hRECs with 100 µM apoEdp in the presence of high glucose significantly reduced the expression of heparanase, shedding of ΔHS, and loss of occludin as detected by Western blot analysis.
117	23284911	Either eye drop treatment of 1% apoEdp topically 4 times a day for 14 consecutive days or intraperitoneal injection (40 mg/kg) of apoEdp daily for 14 consecutive days in an in vivo mouse model of streptozotocin-induced diabetes inhibited the loss of tight junction proteins occludin and zona occludin- 1 (ZO-1).
118	23437353	Effect of 12- or 15-HETE on the levels of zonula occludens protein 1 (ZO-1), reactive oxygen species (ROS), NOX2, pVEGF-R2 and pSHP1 was examined in the presence or absence of inhibitors of NADPH oxidase.
119	23437353	ROS generation and NOX2 expression were also measured in mice retinas. 12- and 15- HETE significantly increased permeability and reduced TER and ZO-1 expression in REC.
120	23437353	Treatment of diabetic mice with baicalein significantly decreased retinal HETE, ICAM-1, VCAM-1, IL-6, ROS generation, and NOX2 expression.
121	23437353	Our findings suggest that 12/15-LOX contributes to vascular hyperpermeability during DR via NADPH oxidase dependent mechanism which involves suppression of protein tyrosine phosphatase and activation of VEGF-R2 signal pathway.
122	23437353	Effect of 12- or 15-HETE on the levels of zonula occludens protein 1 (ZO-1), reactive oxygen species (ROS), NOX2, pVEGF-R2 and pSHP1 was examined in the presence or absence of inhibitors of NADPH oxidase.
123	23437353	ROS generation and NOX2 expression were also measured in mice retinas. 12- and 15- HETE significantly increased permeability and reduced TER and ZO-1 expression in REC.
124	23437353	Treatment of diabetic mice with baicalein significantly decreased retinal HETE, ICAM-1, VCAM-1, IL-6, ROS generation, and NOX2 expression.
125	23437353	Our findings suggest that 12/15-LOX contributes to vascular hyperpermeability during DR via NADPH oxidase dependent mechanism which involves suppression of protein tyrosine phosphatase and activation of VEGF-R2 signal pathway.
126	23579598	Expression of tight junction proteins, occludin and claudin-5, and zonula occludens protein, ZO-1 was also evaluated with immunohistochemistry and Western blot analysis.
127	23579598	BRB breakdown and increased vascular leakage was found in diabetic rats, with increased VEGF expression and down-regulation of occludin, claudin-5, and ZO-1.
128	23579598	CGA treatment effectively preserved the expression of occludin, and decreased VEGF levels, leading to less BRB breakdown and less vascular leakage.
129	23579598	Expression of tight junction proteins, occludin and claudin-5, and zonula occludens protein, ZO-1 was also evaluated with immunohistochemistry and Western blot analysis.
130	23579598	BRB breakdown and increased vascular leakage was found in diabetic rats, with increased VEGF expression and down-regulation of occludin, claudin-5, and ZO-1.
131	23579598	CGA treatment effectively preserved the expression of occludin, and decreased VEGF levels, leading to less BRB breakdown and less vascular leakage.
132	23757509	Fasting insulin, insulin resistance index, plasma LPS level, and ZO1 expression were significantly correlated with GLP2 level.