TY - JOUR
AU - He, Hao
AU - Yang, Wu
AU - Su, Nan
AU - Zhang, Chuankai
AU - Dai, Jianing
AU - Han, Feng
AU - Singhal, Mahak
AU - Bai, Wenjuan
AU - Zhu, Xiaolan
AU - Zhu, Jing
AU - Liu, Zhen
AU - Xia, Wencheng
AU - Liu, Xiaoting
AU - Zhang, Chonghe
AU - Jiang, Kai
AU - Huang, Wenhui
AU - Chen, Dan
AU - Wang, Zhaoyin
AU - He, Xueyang
AU - Kirchhoff, Frank
AU - Li, Zhenyu
AU - Liu, Cong
AU - Huan, Jingning
AU - Wang, Xiaohong
AU - Wei, Wu
AU - Wang, Jing
AU - Augustin, Hellmut
AU - Hu, Junhao
TI - Activating NO-sGC crosstalk in the mouse vascular niche promotes vascular integrity and mitigates acute lung injury.
JO - Journal of experimental medicine
VL - 220
IS - 2
SN - 0022-1007
CY - New York, NY
PB - Rockefeller Univ. Press
M1 - DKFZ-2022-02818
SP - e20211422
PY - 2023
N1 - DKFZ-ZMBH Alliance
AB - Disruption of endothelial cell (ECs) and pericytes interactions results in vascular leakage in acute lung injury (ALI). However, molecular signals mediating EC-pericyte crosstalk have not been systemically investigated, and whether targeting such crosstalk could be adopted to combat ALI remains elusive. Using comparative genome-wide EC-pericyte crosstalk analysis of healthy and LPS-challenged lungs, we discovered that crosstalk between endothelial nitric oxide and pericyte soluble guanylate cyclase (NO-sGC) is impaired in ALI. Indeed, stimulating the NO-sGC pathway promotes vascular integrity and reduces lung edema and inflammation-induced lung injury, while pericyte-specific sGC knockout abolishes this protective effect. Mechanistically, sGC activation suppresses cytoskeleton rearrangement in pericytes through inhibiting VASP-dependent F-actin formation and MRTFA/SRF-dependent de novo synthesis of genes associated with cytoskeleton rearrangement, thereby leading to the stabilization of EC-pericyte interactions. Collectively, our data demonstrate that impaired NO-sGC crosstalk in the vascular niche results in elevated vascular permeability, and pharmacological activation of this crosstalk represents a promising translational therapy for ALI.
KW - Mice
KW - Animals
KW - Soluble Guanylyl Cyclase: genetics
KW - Soluble Guanylyl Cyclase: metabolism
KW - Pericytes
KW - Nitric Oxide: metabolism
KW - Lipopolysaccharides: pharmacology
KW - Acute Lung Injury: genetics
KW - Acute Lung Injury: metabolism
KW - Soluble Guanylyl Cyclase (NLM Chemicals)
KW - Nitric Oxide (NLM Chemicals)
KW - Lipopolysaccharides (NLM Chemicals)
LB - PUB:(DE-HGF)16
C6 - pmid:36350314
DO - DOI:10.1084/jem.20211422
UR - https://inrepo02.dkfz.de/record/182641
ER -