ArticleCardiovascular research2013
Response gene to complement 32 deficiency causes impaired placental angiogenesis in mice.
Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- DOCK2 Deficiency Attenuates Abdominal Aortic Aneurysm Formation-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Developmental diversity and unique sensitivity to injury of lung endothelial subtypes during postnatal growth.iScience · 2023Article
- Regulator of Cell Cycle Protein (RGCC/RGC-32) Protects against Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- RGCC balances self-renewal and neuronal differentiation of neural stem cells in the developing mammalian neocortex.EMBO reports · 2021Article
- RGC-32 and diseases: the first 20 years.Immunologic research · 2019Review
- Dominant-negative inhibition of canonical Notch signaling in trophoblast cells does not disrupt placenta formation.Biology open · 2019Article
- Response Gene to Complement 32 Maintains Blood Pressure Homeostasis by Regulating α-Adrenergic Receptor Expression.Circulation research · 2018Article
- Response gene to complement 32 suppresses adipose tissue thermogenic genes through inhibiting β3-adrenergic receptor/mTORC1 signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- New insights into the roles of RGC-32.Cellular & molecular immunology · 2018Article
- Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Pumilio directs deadenylation-associated translational repression of the cyclin-dependent kinase 1 activator RGC-32.Nucleic acids research · 2018Article
- RGC32 Promotes Bleomycin-Induced Systemic Sclerosis in a Murine Disease Model by Modulating Classically Activated Macrophage Function.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Response Gene to Complement 32 in Vascular Diseases.Frontiers in cardiovascular medicine · 2018Review
- Regulation of Placental Development and Its Impact on Fetal Growth-New Insights From Mouse Models.Frontiers in endocrinology · 2018Review
- The role of complement system in adipose tissue-related inflammation.Immunologic research · 2016Review
- Imaging of Cerebral Amyloid Angiopathy with Bivalent (99m)Tc-Hydroxamamide Complexes.Scientific reports · 2016Article
- The role of complement activation in atherogenesis: the first 40 years.Immunologic research · 2016Review
- RGC-32 Deficiency Protects against Hepatic Steatosis by Reducing Lipogenesis.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
aimsThe objectives of this study are to determine the role of response gene to complement 32 (RGC-32) in the placental angiogenesis during pregnancy and explore the underlying mechanisms. METHODS AND
resultsRGC-32-deficient (RGC32(-/-)) mice were generated from C57BL/6 embryonic stem cells with deletion of exon 2 and 3 of the RGC-32 gene. Most of the RGC32(-/-) mice can survive. However, their body sizes were much smaller compared with their wild-type littermates when they were born. By examining the embryo development and placentas at 16.5 days post-coitum, we found that RGC32(-/-) embryos and foetal placentas were significantly smaller than the wild-type. Further analysis showed that the labyrinth zone of RGC32(-/-) placenta was smaller with defective angiogenesis. Mechanistically, vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2) and placental growth factor (PlGF) were significantly down-regulated in RGC32(-/-) placentas, suggesting that VEGFR2 and PlGF may mediate RGC-32 function in placental angiogenesis. Indeed, knockdown of RGC-32 by shRNA inhibited VEGF-induced endothelial cell proliferation, migration, and tube formation while blocking VEGFR2 expression. RGC-32 appeared to regulate VEGFR2 expression via activation of NF-kB. Moreover, RGC-32 regulated trophoblasts proliferation via control of PlGF expression.
conclusionAbsence of RGC-32 caused foetal growth restriction through interrupting the placental angiogenesis, which was due to the decrease in VEGFR2 expression through the NF-kB-dependent pathway in endothelial cells and PlGF expression in trophoblasts.
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