Open AccessCytokine profile and cytoskeletal changes after herpes simplex virus type 1 infection in human trabecular meshwork cells
Author(s) -
Choi Jin A.,
Ju Hyunhee,
Kim JuEun,
Lee Jiyoung,
Jee Donghyun,
Park Chan Kee,
Paik Soonyoung
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16862
Subject(s) - trabecular meshwork , herpes simplex virus , fibronectin , rhoa , actin , biology , cytokine , inflammation , rho associated protein kinase , microbiology and biotechnology , rho kinase inhibitor , extracellular matrix , immunology , kinase , virus , signal transduction , neuroscience , glaucoma
Uveitis caused by herpes simplex virus (HSV)‐1 is characterized by increased intraocular pressure (IOP) in the presence of anterior chamber inflammation. Despite their clinical significance, the pathogenic changes associated with HSV‐1 infection in trabecular meshwork (TM) cells, the key cell type regulating IOP, have not been completely elucidated. In this study, cytokine array analyses showed a significant stepwise increase in monocyte chemoattractant protein (MCP)‐1 expression upon HSV‐1 infection in TM cells ( p < 0.05). HSV‐1 infection led to downregulation of fibrogenic molecules (fibronectin, α‐smooth muscle actin, connective tissue growth factor and TGF‐β1). Notably, HSV‐1 infection caused a significant increase in actin stress fibres, with a twofold increase in active RhoA, which was enhanced by treatment with TGF‐β1 and inhibited by treatment with the Rho‐kinase inhibitor, Y‐27632. TM cells treated with MCP‐1 exhibited a dose‐dependent increase in actin stress fibres compared to untreated TM cells. Our study suggests that HSV‐1 infection in TM cells increases cell contractile activity rather than fibrotic changes in the extracellular matrix (ECM) components. Taken together, these observations demonstrate the enhanced expression of MCP‐1 and TM cell contractile activity upon HSV‐1 infection and events with potential implications for the pathobiology of abrupt IOP elevation in HSV‐1 anterior uveitis.