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Expression patterns of STAT3, ERK and estrogen-receptor α are associated with development and histologic severity of hepatic steatosis: a retrospective study

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dc.contributor.authorChoi, Euno-
dc.contributor.authorKim, Won-
dc.contributor.authorJoo, Sae Kyung-
dc.contributor.authorPark, Sunyoung-
dc.contributor.authorPark, Jeong Hwan-
dc.contributor.authorKang, Yun Kyung-
dc.contributor.authorJin, So-Young-
dc.contributor.authorChang, Mee Soo-
dc.date.accessioned2018-05-15T05:06:58Z-
dc.date.available2018-05-15T14:09:08Z-
dc.date.issued2018-04-03-
dc.identifier.citationDiagnostic Pathology, 13(1):23ko_KR
dc.identifier.issn1746-1596-
dc.identifier.urihttps://hdl.handle.net/10371/139764-
dc.description.abstractBackground
Hepatic steatosis renders hepatocytes vulnerable to injury, resulting in the progression of preexisting liver disease. Previous animal and cell culture studies implicated mammalian target of rapamycin (mTOR), signal transducer and activator of transcription-3 (STAT3), extracellular signal-regulated kinase (ERK) and estrogen-receptor α in the pathogenesis of hepatic steatosis and disease progression. However, to date there have been few studies performed using human liver tissue to study hepatic steatosis. We examined the expression patterns of mTOR, STAT3, ERK and estrogen-receptor α in liver tissues from patients diagnosed with hepatic steatosis.

Methods
We reviewed the clinical and histomorphological features of 29 patients diagnosed with hepatic steatosis: 18 with non-alcoholic fatty liver disease (NAFLD), 11 with alcoholic fatty acid disease (AFLD), and a control group (16 biliary cysts and 22 hepatolithiasis). Immunohistochemistry was performed on liver tissue using an automated immunostainer. The histologic severity of hepatic steatosis was evaluated by assessing four key histomorphologic parameters common to NAFLD and AFLD: steatosis, lobular inflammation, ballooning degeneration and fibrosis.

Results
mTOR, phosphorylated STAT3, phosphorylated pERK, estrogen-receptor α were found to be more frequently expressed in the hepatic steatosis group than in the control group. Specifically, mTOR was expressed in 78% of hepatocytes, and ERK in 100% of hepatic stellate cells, respectively, in patients with NAFLD. Interestingly, estrogen-receptor α was diffusely expressed in hepatocytes in all NALFD cases. Phosphorylated (active) STAT3 was expressed in 73% of hepatocytes and 45% of hepatic stellate cells in patients with AFLD, and phosphorylated (active) ERK was expressed in hepatic stellate cells in all AFLD cases. Estrogen-receptor α was expressed in all AFLD cases (focally in 64% of AFLD cases, and diffusely in 36%). Phosphorylated STAT3 expression in hepatocytes and hepatic stellate cells correlated with severe lobular inflammation, severe ballooning degeneration and advanced fibrosis, whereas diffusely expressed estrogen-receptor α correlated with a mild stage of fibrosis.

Conclusions
Our data indicate ERK activation and estrogen-receptor α may be relevant in the development of hepatic steatosis. However, diffuse expression of estrogen-receptor α would appear to impede disease progression, including hepatic fibrosis. Finally, phosphorylated STAT3 may also contribute to disease progression.
ko_KR
dc.description.sponsorshipThis work was supported by the Basic Science Research Program of the National Research Foundation of Korea, which is funded by the Ministry of Education (2016R1D1A1B01010316).ko_KR
dc.language.isoenko_KR
dc.publisherBioMed Centralko_KR
dc.subjectHepatic steatosisko_KR
dc.subjectNon-alcoholicko_KR
dc.subjectAlcoholicko_KR
dc.subjectmTORko_KR
dc.subjectpSTAT3ko_KR
dc.subjectpERKko_KR
dc.subjectEstrogen-receptor αko_KR
dc.titleExpression patterns of STAT3, ERK and estrogen-receptor α are associated with development and histologic severity of hepatic steatosis: a retrospective studyko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor최은오-
dc.contributor.AlternativeAuthor김원-
dc.contributor.AlternativeAuthor주세경-
dc.contributor.AlternativeAuthor박선영-
dc.contributor.AlternativeAuthor박정환-
dc.contributor.AlternativeAuthor강윤경-
dc.contributor.AlternativeAuthor진소영-
dc.contributor.AlternativeAuthor장미수-
dc.identifier.doi10.1186/s13000-018-0698-8-
dc.rights.holderThe Author(s).-
dc.date.updated2018-04-08T03:29:21Z-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Pathology (병리학전공)Journal Papers (저널논문_병리학전공)
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