Loss of laminin-γ1 in pericytes impairs microvascular function and cognition

Blood-brain barrier (BBB) disruption correlates with lesion burden and cognitive dysfunction in cerebral small vessel disease (CSVD). Laminin, highly produced by pericytes in the brain, maintains BBB integrity. However, it remains unclear if laminin dysregulation contributes to the pathogenesis of CSVD. Here, we show that mice lacking laminin-γ1 in pericytes, smooth muscle cells, and fibroblasts (PKO) develop age-dependent BBB disruption via both paracellular and transcellular mechanisms. In contrast, loss of laminin-γ1 in smooth muscle cells or fibroblasts fails to affect BBB integrity. In addition, the PKO mice exhibit pericyte loss, thickened basal lamina, increased brain stiffness, followed by brain clearance defect, synaptic loss, and cognitive impairment. Together, these results demonstrate that loss of pericytic laminin-γ1 induces progressive vascular dysfunction and several features of CSVD, including brain stiffness, synaptic loss, and cognitive impairment, highlighting a potential role of laminin-γ1 dysregulation in the pathogenesis of CSVD.

Authors

Institutions

Publication Details

Journal
Cell Reports
Published
2026-08-27
DOI
https://doi.org/10.1016/j.celrep.2026.117904
Primary Topic
Barrier Structure and Function Studies
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Loss of laminin-γ1 in pericytes impairs microvascular function and cognition

Meisam Asgari, Ava Nasrollahi, Yao Yao, Cecilia Martin et al.
Cell Reports
Barrier Structure and Function Studies
article

Loss of laminin-γ1 in pericytes impairs microvascular function and cognition

Meisam Asgari, Ava Nasrollahi, Yao Yao, Cecilia Martin, Jingsong Ruan, Andy Y. Shih
article en

Abstract

Blood-brain barrier (BBB) disruption correlates with lesion burden and cognitive dysfunction in cerebral small vessel disease (CSVD). Laminin, highly produced by pericytes in the brain, maintains BBB integrity. However, it remains unclear if laminin dysregulation contributes to the pathogenesis of CSVD. Here, we show that mice lacking laminin-γ1 in pericytes, smooth muscle cells, and fibroblasts (PKO) develop age-dependent BBB disruption via both paracellular and transcellular mechanisms. In contrast, loss of laminin-γ1 in smooth muscle cells or fibroblasts fails to affect BBB integrity. In addition, the PKO mice exhibit pericyte loss, thickened basal lamina, increased brain stiffness, followed by brain clearance defect, synaptic loss, and cognitive impairment. Together, these results demonstrate that loss of pericytic laminin-γ1 induces progressive vascular dysfunction and several features of CSVD, including brain stiffness, synaptic loss, and cognitive impairment, highlighting a potential role of laminin-γ1 dysregulation in the pathogenesis of CSVD.

Cell ReportsVol. 45(9)
Seattle Children's Hospital (US), University of Washington (US), University of South Florida (US), Seattle Children's Hospital (US)
Alzheimer's Association, American Heart Association, Fondation Leducq, National Institute on Aging, National Heart, Lung, and Blood Institute, National Institute of Neurological Disorders and Stroke
Good health and well-being
Openalex Percentile: Top 13%
Barrier Structure and Function Studies
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.