Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0023890 (
cirrhosis
)
42,195
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The aim of the present study was to elucidate the effect of
transmembrane protein 16A
(
TMEM16A
) on portal vein smooth muscle cell (PVSMC) proliferation associated with portal vein remodeling in portal hypertension (PHT). Sprague-Dawley rats were subjected to bile duct ligation to establish a rat model of
liver cirrhosis
and PHT. Sham-operated animals served as controls. At 8 weeks after bile duct ligation, the extent of liver fibrosis and the portal vein wall thickness were assessed using hematoxylin-eosin staining. The protein expression levels of
TMEM16A
, extracellular signal-regulated kinase 1 and 2 (ERK1/2) and phosphorylated ERK1/2 (p-ERK1/2) in the portal vein were detected by immunohistochemistry and western blotting.
In vitro
, the lentivirus vectors were constructed and transfected into PVSMCs to upregulate the expression of
TMEM16A
. Isolated rat primary PVSMCs were treated with a small molecule inhibitor of
TMEM16A
, T16A-inhA01. Cell cycle was detected by flow cytometry. The activity of
TMEM16A
in the portal vein isolated from bile duct ligated rats was decreased, while the expression level of p-ERK1/2 was increased. However,
in vitro
, upregulation of
TMEM16A
promoted the proliferation PVSMCs, while inhibition of
TMEM16A
channels inhibited the proliferation of PVSMCs. The results indicated that
TMEM16A
contributes to PVSMCs proliferation
in vitro
, but
in vivo
, it may be a negative regulator of cell proliferation influenced by numerous factors.
...
PMID:TMEM16A regulates portal vein smooth muscle cell proliferation in portal hypertension. 2943 96
