인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
DBpia AI
AI 에이전트
AI 아이디어
AI 리더
AI 뷰어
Citeasy
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지원사업
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커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Vascular cells express various G-protein-coupled receptors (GPCRs) with yet unknown function, among them orphan receptor GPR153. GPR153 was upregulated in smooth muscle cells (SMCs) in response to injury, and knockdown of GPR153 resulted in reduced proliferation and mildly altered differentiation in human SMCs. Mice with tamoxifen-inducible, SMC-specific GPR153 deficiency were partially protected against ligation-induced neointima formation, and their SMCs were characterized by reduced proliferation and dedifferentiation. Mechanistically, we show that GPR153 negatively regulates cellular cAMP levels, and thus the absence of GPR153 leads to an increase in CREB phosphorylation, reduced YAP/TAZ levels, and diminished NF-κB activation. Interestingly, a similar role of GPR153 was observed in endothelial cells (ECs), where loss of GPR153 resulted in reduced inflammatory gene expression and protected mice with EC-specific GPR153 deficiency in models of neuroinflammation and stroke. Taken together, orphan receptor GPR153 facilitates pro-inflammatory and pro-proliferative gene expression in ECs and SMCs by controlling cellular cAMP levels, thereby contributing to inflammation and vascular remodeling.
#Cell biology
#Neointima
#Signal transduction
#Receptor
#Gene knockdown
#Inflammation
#Downregulation and upregulation
#Phosphorylation
#CREB
#G protein-coupled receptor
#Neuroinflammation
#Biology
#Chemistry
#Cancer research
#Internal medicine
#Immunology
#Medicine
#Transcription factor
#Gene
#Biochemistry
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