Ignet

Gene Information

Gene symbol: SEMA3A

Gene name: sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3A

HGNC ID: 10723

Synonyms: SEMA1, SemD, coll-1, Hsema-I

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	COL1A1	1 hits
3	COL4A4	1 hits
4	CXCL12	1 hits
5	EGF	1 hits
6	GDNF	1 hits
7	JUN	1 hits
8	KCNQ1OT1	1 hits
9	KDR	1 hits
10	MAPK8	1 hits
11	MARCH8	1 hits
12	MICAL1	1 hits
13	MIRN15B	1 hits
14	MIRN203	1 hits
15	MMP9	1 hits
16	NPHS1	1 hits
17	NRP1	1 hits
18	NRP2	1 hits
19	SEMA3C	1 hits
20	SEMA3F	1 hits
21	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	12617854	Neuropilin 1 and 2 (NP-1, NP-2) are natural ligands for semaphorins 3A and 3F, respectively.
2	12617854	NP-1 is also a co-receptor for vascular endothelial growth factor (VEGF) required for normal vascular development.
3	12617854	To examine whether semaphorins could modulate VEGF endothelial cell guidance cues in the developing kidney, we studied the expression of semaphorin 3A and semaphorin 3F and their receptors NP-1 and NP-2 in the kidney during ontogeny using Northern blot analysis, in situ hybridization, Western blot analysis and immunohistochemistry.
4	12617854	Semaphorin 3A and 3F are expressed by podocytes and tubules whereas their receptors NP-1 and NP-2 are localized to endothelial cells.
5	12617854	The distribution of the receptors NP-1 and NP-2 in endothelial cells and developing vessels is complementary to that of the ligands in adjacent epithelial cells during kidney development.
6	12617854	Neuropilin 1 and 2 (NP-1, NP-2) are natural ligands for semaphorins 3A and 3F, respectively.
7	12617854	NP-1 is also a co-receptor for vascular endothelial growth factor (VEGF) required for normal vascular development.
8	12617854	To examine whether semaphorins could modulate VEGF endothelial cell guidance cues in the developing kidney, we studied the expression of semaphorin 3A and semaphorin 3F and their receptors NP-1 and NP-2 in the kidney during ontogeny using Northern blot analysis, in situ hybridization, Western blot analysis and immunohistochemistry.
9	12617854	Semaphorin 3A and 3F are expressed by podocytes and tubules whereas their receptors NP-1 and NP-2 are localized to endothelial cells.
10	12617854	The distribution of the receptors NP-1 and NP-2 in endothelial cells and developing vessels is complementary to that of the ligands in adjacent epithelial cells during kidney development.
11	14516677	Neuropilin 1 and 2 (NP-1, NP-2) are natural ligands for semaphorins 3A and 3F, respectively.
12	14516677	NP-1 is also a co-receptor for vascular endothelial growth factor (VEGF) required for normal vascular development.
13	14516677	To examine whether semaphorins could modulate VEGF endothelial cell guidance cues in the developing kidney, we studied the expression of semaphorin 3A and semaphorin 3F and their receptors NP-1 and NP-2 in the kidney during ontogeny using Northern blot analysis, in situ hybridization, Western blot analysis and immunohistochemistry.
14	14516677	Semaphorin 3A and 3F are expressed by podocytes and tubules whereas their receptors NP-1 and NP-2 are localized to endothelial cells.
15	14516677	The distribution of the receptors NP-1 and NP-2 in endothelial cells and developing vessels is complementary to that of the ligands in adjacent epithelial cells during kidney development.
16	14516677	Neuropilin 1 and 2 (NP-1, NP-2) are natural ligands for semaphorins 3A and 3F, respectively.
17	14516677	NP-1 is also a co-receptor for vascular endothelial growth factor (VEGF) required for normal vascular development.
18	14516677	To examine whether semaphorins could modulate VEGF endothelial cell guidance cues in the developing kidney, we studied the expression of semaphorin 3A and semaphorin 3F and their receptors NP-1 and NP-2 in the kidney during ontogeny using Northern blot analysis, in situ hybridization, Western blot analysis and immunohistochemistry.
19	14516677	Semaphorin 3A and 3F are expressed by podocytes and tubules whereas their receptors NP-1 and NP-2 are localized to endothelial cells.
20	14516677	The distribution of the receptors NP-1 and NP-2 in endothelial cells and developing vessels is complementary to that of the ligands in adjacent epithelial cells during kidney development.
21	18249526	Additional studies revealed that SEMA3A effects on ureteric bud branching involve downregulation of glial cell-line derived neurotrophic factor (GDNF) signaling, competition with vascular endothelial growth factor A (VEGF-A) and decreased activity of Akt survival pathways.
22	18443354	Compared with controls, immunohistochemistry revealed that kidneys from HIV-1-transgenic mice (Tg26) and from patients with HIVAN had greater expression of both VEGF and its transcriptional regulator, hypoxia-inducible factor 2alpha (HIF-2alpha).
23	18443354	Similarly, mRNA and protein levels of VEGF and HIF-2alpha were increased in HIV-infected podocytes in vitro, and this transcriptional upregulation was found to be stimulated by the HIV viral protein Nef in a Src kinase-and Stat3-dependent manner.
24	18443354	HIV-1 also upregulated VEGFR2 and its co-receptor neuropilin-1 and suppressed the expression of semaphorin 3a in the podocyte.
25	18443354	Exogenous VEGF stimulated proliferation and de-differentiation of podocytes, which are features of collapsing FSGS, and VEGFR2 neutralizing antibodies reversed these features in podocytes infected with HIV-1 or isolated from Tg26 mice.
26	18443354	In conclusion, HIV-1 induces VEGF and VEGFR2 expression in podocytes, and this may be a critical step in the pathogenesis of HIVAN.
27	21336944	In addition, Sema3a is a negative regulator of ureteric bud branching, whereas Sema3c is a positive regulator of ureteric bud and endothelial cell branching morphogenesis.
28	23954273	Excess podocyte semaphorin-3A leads to glomerular disease involving plexinA1-nephrin interaction.
29	23954273	Mechanistically, excess Sema3a induces dysregulation of nephrin, matrix metalloproteinase 9, and αvβ3 integrin in vivo.
30	23954273	We identified a novel direct interaction between the Sema3a signaling receptor plexinA1 and nephrin, linking extracellular Sema3a signals to the slit-diaphragm signaling complex.
31	23954273	Our findings demonstrate a crosstalk between Sema3a and nephrin signaling pathways that is functionally relevant both in vivo and in vitro.
32	23954273	Excess podocyte semaphorin-3A leads to glomerular disease involving plexinA1-nephrin interaction.
33	23954273	Mechanistically, excess Sema3a induces dysregulation of nephrin, matrix metalloproteinase 9, and αvβ3 integrin in vivo.
34	23954273	We identified a novel direct interaction between the Sema3a signaling receptor plexinA1 and nephrin, linking extracellular Sema3a signals to the slit-diaphragm signaling complex.
35	23954273	Our findings demonstrate a crosstalk between Sema3a and nephrin signaling pathways that is functionally relevant both in vivo and in vitro.
36	23954273	Excess podocyte semaphorin-3A leads to glomerular disease involving plexinA1-nephrin interaction.
37	23954273	Mechanistically, excess Sema3a induces dysregulation of nephrin, matrix metalloproteinase 9, and αvβ3 integrin in vivo.
38	23954273	We identified a novel direct interaction between the Sema3a signaling receptor plexinA1 and nephrin, linking extracellular Sema3a signals to the slit-diaphragm signaling complex.
39	23954273	Our findings demonstrate a crosstalk between Sema3a and nephrin signaling pathways that is functionally relevant both in vivo and in vitro.
40	23954273	Excess podocyte semaphorin-3A leads to glomerular disease involving plexinA1-nephrin interaction.
41	23954273	Mechanistically, excess Sema3a induces dysregulation of nephrin, matrix metalloproteinase 9, and αvβ3 integrin in vivo.
42	23954273	We identified a novel direct interaction between the Sema3a signaling receptor plexinA1 and nephrin, linking extracellular Sema3a signals to the slit-diaphragm signaling complex.
43	23954273	Our findings demonstrate a crosstalk between Sema3a and nephrin signaling pathways that is functionally relevant both in vivo and in vitro.
44	24464477	Excess sema3a causes foot process effacement, glomerular basement lamination, and endothelial damage in vivo, and disrupts cell autonomously podocyte shape by down-regulating nephrin and inhibiting αvβ3 integrin.
45	24464477	We identified a novel direct interaction between nephrin and plexinA1, the sema3a signaling receptor.
46	24464477	Nephrin-plexinA1 interaction links the slit-diaphragm signaling complex to extracellular sema3a signals.
47	24464477	Excess sema3a causes foot process effacement, glomerular basement lamination, and endothelial damage in vivo, and disrupts cell autonomously podocyte shape by down-regulating nephrin and inhibiting αvβ3 integrin.
48	24464477	We identified a novel direct interaction between nephrin and plexinA1, the sema3a signaling receptor.
49	24464477	Nephrin-plexinA1 interaction links the slit-diaphragm signaling complex to extracellular sema3a signals.
50	24464477	Excess sema3a causes foot process effacement, glomerular basement lamination, and endothelial damage in vivo, and disrupts cell autonomously podocyte shape by down-regulating nephrin and inhibiting αvβ3 integrin.
51	24464477	We identified a novel direct interaction between nephrin and plexinA1, the sema3a signaling receptor.
52	24464477	Nephrin-plexinA1 interaction links the slit-diaphragm signaling complex to extracellular sema3a signals.
53	25475434	In diabetic mice, Sema3a(+) exacerbates laminin and collagen IV accumulation in Kimmelstiel-Wilson-like glomerular nodules and causes diffuse podocyte foot process effacement and F-actin collapse via nephrin, αvβ3 integrin, and MICAL1 interactions with plexinA1.
54	25475434	MICAL1 knockdown and sema3a inhibition render podocytes not susceptible to sema3a-induced shape changes, indicating that MICAL1 mediates sema3a-induced podocyte F-actin collapse.
55	25475434	In diabetic mice, Sema3a(+) exacerbates laminin and collagen IV accumulation in Kimmelstiel-Wilson-like glomerular nodules and causes diffuse podocyte foot process effacement and F-actin collapse via nephrin, αvβ3 integrin, and MICAL1 interactions with plexinA1.
56	25475434	MICAL1 knockdown and sema3a inhibition render podocytes not susceptible to sema3a-induced shape changes, indicating that MICAL1 mediates sema3a-induced podocyte F-actin collapse.
57	26863327	VEGF, ANGPT, EGF, SEMA3A, TGF-β, and CXCL12 signal in paracrine fashions between the podocytes, endothelium, and mesangium associated with the glomerular capillary bed to maintain filtration barrier function.
58	27787866	Podocyte Shape Regulation by Semaphorin 3A and MICAL-1.
59	27787866	MICAL-1 is an actin-binding protein that mediates Sema3A signals in podocytes.
60	27787866	Podocyte Shape Regulation by Semaphorin 3A and MICAL-1.
61	27787866	MICAL-1 is an actin-binding protein that mediates Sema3A signals in podocytes.
62	31025335	miR-15b-5p ameliorated high glucose-induced podocyte injury through repressing apoptosis, oxidative stress, and inflammatory responses by targeting Sema3A.
63	31025335	Meanwhile, forced expression of miR-15b-5p apparently restrained HG-triggered apoptosis of podocytes, concomitant with downregulated in the proapoptotic protein markers Bax and cleavage caspase-3, and upregulated the antiapoptotic protein Bcl-2.
64	31025335	Simultaneously, introduction of miR-15b-5p repressed HG-induced oxidative stress damage in HG-treated podocytes, as evidenced by reduced MDA content, NOX4 expression, and enhanced activities of superoxide dismutase and catalase.
65	31025335	Moreover, enforced expression of miR-15b-5p remarkably restrained the HG-stimulated inflammatory response, as reflected by attenuated the level of the cytokines IL-1β, TNF-α, and IL-6.
66	31025335	More important, we also identified Sema3A as a direct target of miR-15b-5p.
67	31025335	Reverse transcription polymerase chain reaction and western blot subsequently confirmed that miR-15b-5p negatively modulated the level of Sema3A.
68	31025335	Mechanically, overexpression of Sema3A impeded the beneficial effects of miR-15b-5p on HG-mediated apoptosis, oxidative stress, and inflammatory response.
69	31025335	Altogether, these findings manifested that miR-15b-5p protectively antagonized HG-triggered podocyte damage through relieving HG-induced apoptosis, oxidative stress, and inflammatory process in podocytes by targeting Sema3A, suggesting that miR-15b-5p might be a new therapeutic agent to improve management of DN.
70	31025335	miR-15b-5p ameliorated high glucose-induced podocyte injury through repressing apoptosis, oxidative stress, and inflammatory responses by targeting Sema3A.
71	31025335	Meanwhile, forced expression of miR-15b-5p apparently restrained HG-triggered apoptosis of podocytes, concomitant with downregulated in the proapoptotic protein markers Bax and cleavage caspase-3, and upregulated the antiapoptotic protein Bcl-2.
72	31025335	Simultaneously, introduction of miR-15b-5p repressed HG-induced oxidative stress damage in HG-treated podocytes, as evidenced by reduced MDA content, NOX4 expression, and enhanced activities of superoxide dismutase and catalase.
73	31025335	Moreover, enforced expression of miR-15b-5p remarkably restrained the HG-stimulated inflammatory response, as reflected by attenuated the level of the cytokines IL-1β, TNF-α, and IL-6.
74	31025335	More important, we also identified Sema3A as a direct target of miR-15b-5p.
75	31025335	Reverse transcription polymerase chain reaction and western blot subsequently confirmed that miR-15b-5p negatively modulated the level of Sema3A.
76	31025335	Mechanically, overexpression of Sema3A impeded the beneficial effects of miR-15b-5p on HG-mediated apoptosis, oxidative stress, and inflammatory response.
77	31025335	Altogether, these findings manifested that miR-15b-5p protectively antagonized HG-triggered podocyte damage through relieving HG-induced apoptosis, oxidative stress, and inflammatory process in podocytes by targeting Sema3A, suggesting that miR-15b-5p might be a new therapeutic agent to improve management of DN.
78	31025335	miR-15b-5p ameliorated high glucose-induced podocyte injury through repressing apoptosis, oxidative stress, and inflammatory responses by targeting Sema3A.
79	31025335	Meanwhile, forced expression of miR-15b-5p apparently restrained HG-triggered apoptosis of podocytes, concomitant with downregulated in the proapoptotic protein markers Bax and cleavage caspase-3, and upregulated the antiapoptotic protein Bcl-2.
80	31025335	Simultaneously, introduction of miR-15b-5p repressed HG-induced oxidative stress damage in HG-treated podocytes, as evidenced by reduced MDA content, NOX4 expression, and enhanced activities of superoxide dismutase and catalase.
81	31025335	Moreover, enforced expression of miR-15b-5p remarkably restrained the HG-stimulated inflammatory response, as reflected by attenuated the level of the cytokines IL-1β, TNF-α, and IL-6.
82	31025335	More important, we also identified Sema3A as a direct target of miR-15b-5p.
83	31025335	Reverse transcription polymerase chain reaction and western blot subsequently confirmed that miR-15b-5p negatively modulated the level of Sema3A.
84	31025335	Mechanically, overexpression of Sema3A impeded the beneficial effects of miR-15b-5p on HG-mediated apoptosis, oxidative stress, and inflammatory response.
85	31025335	Altogether, these findings manifested that miR-15b-5p protectively antagonized HG-triggered podocyte damage through relieving HG-induced apoptosis, oxidative stress, and inflammatory process in podocytes by targeting Sema3A, suggesting that miR-15b-5p might be a new therapeutic agent to improve management of DN.
86	31025335	miR-15b-5p ameliorated high glucose-induced podocyte injury through repressing apoptosis, oxidative stress, and inflammatory responses by targeting Sema3A.
87	31025335	Meanwhile, forced expression of miR-15b-5p apparently restrained HG-triggered apoptosis of podocytes, concomitant with downregulated in the proapoptotic protein markers Bax and cleavage caspase-3, and upregulated the antiapoptotic protein Bcl-2.
88	31025335	Simultaneously, introduction of miR-15b-5p repressed HG-induced oxidative stress damage in HG-treated podocytes, as evidenced by reduced MDA content, NOX4 expression, and enhanced activities of superoxide dismutase and catalase.
89	31025335	Moreover, enforced expression of miR-15b-5p remarkably restrained the HG-stimulated inflammatory response, as reflected by attenuated the level of the cytokines IL-1β, TNF-α, and IL-6.
90	31025335	More important, we also identified Sema3A as a direct target of miR-15b-5p.
91	31025335	Reverse transcription polymerase chain reaction and western blot subsequently confirmed that miR-15b-5p negatively modulated the level of Sema3A.
92	31025335	Mechanically, overexpression of Sema3A impeded the beneficial effects of miR-15b-5p on HG-mediated apoptosis, oxidative stress, and inflammatory response.
93	31025335	Altogether, these findings manifested that miR-15b-5p protectively antagonized HG-triggered podocyte damage through relieving HG-induced apoptosis, oxidative stress, and inflammatory process in podocytes by targeting Sema3A, suggesting that miR-15b-5p might be a new therapeutic agent to improve management of DN.
94	31025335	miR-15b-5p ameliorated high glucose-induced podocyte injury through repressing apoptosis, oxidative stress, and inflammatory responses by targeting Sema3A.
95	31025335	Meanwhile, forced expression of miR-15b-5p apparently restrained HG-triggered apoptosis of podocytes, concomitant with downregulated in the proapoptotic protein markers Bax and cleavage caspase-3, and upregulated the antiapoptotic protein Bcl-2.
96	31025335	Simultaneously, introduction of miR-15b-5p repressed HG-induced oxidative stress damage in HG-treated podocytes, as evidenced by reduced MDA content, NOX4 expression, and enhanced activities of superoxide dismutase and catalase.
97	31025335	Moreover, enforced expression of miR-15b-5p remarkably restrained the HG-stimulated inflammatory response, as reflected by attenuated the level of the cytokines IL-1β, TNF-α, and IL-6.
98	31025335	More important, we also identified Sema3A as a direct target of miR-15b-5p.
99	31025335	Reverse transcription polymerase chain reaction and western blot subsequently confirmed that miR-15b-5p negatively modulated the level of Sema3A.
100	31025335	Mechanically, overexpression of Sema3A impeded the beneficial effects of miR-15b-5p on HG-mediated apoptosis, oxidative stress, and inflammatory response.
101	31025335	Altogether, these findings manifested that miR-15b-5p protectively antagonized HG-triggered podocyte damage through relieving HG-induced apoptosis, oxidative stress, and inflammatory process in podocytes by targeting Sema3A, suggesting that miR-15b-5p might be a new therapeutic agent to improve management of DN.
102	32521824	In addition, c-Jun N-terminal kinase (JNK), known as a downstream of SEMA3A signaling, was activated in Dox-injected mouse podocytes while SEMA3A-I treatment partially blocked the activation.
103	32521824	In vitro, SEMA3A-I protected against Dox-induced podocyte apoptosis and recombinant SEMA3A caused podocyte apoptosis with activation of JNK signaling.
104	32521824	JNK inhibitor, SP600125, attenuated SEMA3A-induced podocyte apoptosis, indicating that the JNK pathway would be involved in SEMA3A-induced podocyte apoptosis.
105	32521824	In addition, c-Jun N-terminal kinase (JNK), known as a downstream of SEMA3A signaling, was activated in Dox-injected mouse podocytes while SEMA3A-I treatment partially blocked the activation.
106	32521824	In vitro, SEMA3A-I protected against Dox-induced podocyte apoptosis and recombinant SEMA3A caused podocyte apoptosis with activation of JNK signaling.
107	32521824	JNK inhibitor, SP600125, attenuated SEMA3A-induced podocyte apoptosis, indicating that the JNK pathway would be involved in SEMA3A-induced podocyte apoptosis.
108	32521824	In addition, c-Jun N-terminal kinase (JNK), known as a downstream of SEMA3A signaling, was activated in Dox-injected mouse podocytes while SEMA3A-I treatment partially blocked the activation.
109	32521824	In vitro, SEMA3A-I protected against Dox-induced podocyte apoptosis and recombinant SEMA3A caused podocyte apoptosis with activation of JNK signaling.
110	32521824	JNK inhibitor, SP600125, attenuated SEMA3A-induced podocyte apoptosis, indicating that the JNK pathway would be involved in SEMA3A-induced podocyte apoptosis.
111	33817280	MiR-203-3p inhibits the oxidative stress, inflammatory responses and apoptosis of mice podocytes induced by high glucose through regulating Sema3A expression.
112	33817280	The expression levels of miR-203-3p, Semaphorin 3A (Sema3A) and inflammatory cytokines were detected by quantitative real-time polymerase chain reaction.
113	33817280	Functionally, Sema3A was a target of miR-203-3p, and Sema3A overexpression reversed the inhibitory effect of miR-203-3p on HG-induced podocyte injury.
114	33817280	Our findings revealed that miR-203-3p alleviated the podocyte injury induced by HG via regulating Sema3A expression, suggesting that miR-203-3p might be a new therapeutic target to improve the progression of DN.
115	33817280	MiR-203-3p inhibits the oxidative stress, inflammatory responses and apoptosis of mice podocytes induced by high glucose through regulating Sema3A expression.
116	33817280	The expression levels of miR-203-3p, Semaphorin 3A (Sema3A) and inflammatory cytokines were detected by quantitative real-time polymerase chain reaction.
117	33817280	Functionally, Sema3A was a target of miR-203-3p, and Sema3A overexpression reversed the inhibitory effect of miR-203-3p on HG-induced podocyte injury.
118	33817280	Our findings revealed that miR-203-3p alleviated the podocyte injury induced by HG via regulating Sema3A expression, suggesting that miR-203-3p might be a new therapeutic target to improve the progression of DN.
119	33817280	MiR-203-3p inhibits the oxidative stress, inflammatory responses and apoptosis of mice podocytes induced by high glucose through regulating Sema3A expression.
120	33817280	The expression levels of miR-203-3p, Semaphorin 3A (Sema3A) and inflammatory cytokines were detected by quantitative real-time polymerase chain reaction.
121	33817280	Functionally, Sema3A was a target of miR-203-3p, and Sema3A overexpression reversed the inhibitory effect of miR-203-3p on HG-induced podocyte injury.
122	33817280	Our findings revealed that miR-203-3p alleviated the podocyte injury induced by HG via regulating Sema3A expression, suggesting that miR-203-3p might be a new therapeutic target to improve the progression of DN.
123	33817280	MiR-203-3p inhibits the oxidative stress, inflammatory responses and apoptosis of mice podocytes induced by high glucose through regulating Sema3A expression.
124	33817280	The expression levels of miR-203-3p, Semaphorin 3A (Sema3A) and inflammatory cytokines were detected by quantitative real-time polymerase chain reaction.
125	33817280	Functionally, Sema3A was a target of miR-203-3p, and Sema3A overexpression reversed the inhibitory effect of miR-203-3p on HG-induced podocyte injury.
126	33817280	Our findings revealed that miR-203-3p alleviated the podocyte injury induced by HG via regulating Sema3A expression, suggesting that miR-203-3p might be a new therapeutic target to improve the progression of DN.
127	34997887	KCNQ1OT1 inhibition alleviates high glucose-induced podocyte injury by adsorbing miR-23b-3p and regulating Sema3A.