Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis

BackgroundGender-related factors have explained the higher prevalence of autoimmune diseases in women. Sex hormones play a key role in the immune system and parenchymal cells function; therefore, these hormones can be important in the pathogenesis of autoimmune diseases as a risk or beneficial facto...

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Autores principales:	Fatemeh Vafashoar, Kazem Mousavizadeh, Hadi Poormoghim, Amir Haghighi, Salar Pashangzadeh, Nazanin Mojtabavi
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	progesterone systemic sclerosis scleroderma lung fibrosis bleomycin Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/d3bf2047cca3459596c626d0437b4247
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spelling	oai:doaj.org-article:d3bf2047cca3459596c626d0437b42472021-12-01T13:37:12ZProgesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis1664-322410.3389/fimmu.2021.742227https://doaj.org/article/d3bf2047cca3459596c626d0437b42472021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.742227/fullhttps://doaj.org/toc/1664-3224BackgroundGender-related factors have explained the higher prevalence of autoimmune diseases in women. Sex hormones play a key role in the immune system and parenchymal cells function; therefore, these hormones can be important in the pathogenesis of autoimmune diseases as a risk or beneficial factor. Lung fibrosis is the main cause of mortality in systemic sclerosis, a female predominant autoimmune disease. The objective of this study was to examine the effect of progesterone on lung fibrosis in a mouse model of systemic sclerosis.MethodsMice with bleomycin-induced lung fibrosis treated with progesterone subcutaneously for 21 and 28 days. Blood was collected for hormone and cytokine measurement at the end of treatment then, skin and lung tissues were harvested for histological assessment, gene expression, cytokine, hydroxyproline, and gelatinase measurement.ResultsTrichrome staining and hydroxyproline measurements showed that progesterone treatment increased the content of collagen in fibrotic and normal lung tissues. Progesterone increased α-SMA (P < 0.01), TGF- β (P < 0.05) and decreased MMP9 (P < 0.05) in fibrotic lung tissues. Also progesterone treatment decreased the gene expression of Col1a2 (P <0.05), Ctgf (P <01), End1 (0.001) in bleomycin- injured lung tissues. The serum level of TNF-α was decreased, but the serum level of cortisol was increased by progesterone treatment in fibrotic mice (P< 0.05).ConclusionOur results showed that progesterone aggravates lung fibrosis in a mouse model of systemic sclerosis.Fatemeh VafashoarFatemeh VafashoarKazem MousavizadehHadi PoormoghimAmir HaghighiSalar PashangzadehSalar PashangzadehNazanin MojtabaviNazanin MojtabaviFrontiers Media S.A.articleprogesteronesystemic sclerosissclerodermalungfibrosisbleomycinImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	progesterone systemic sclerosis scleroderma lung fibrosis bleomycin Immunologic diseases. Allergy RC581-607
spellingShingle	progesterone systemic sclerosis scleroderma lung fibrosis bleomycin Immunologic diseases. Allergy RC581-607 Fatemeh Vafashoar Fatemeh Vafashoar Kazem Mousavizadeh Hadi Poormoghim Amir Haghighi Salar Pashangzadeh Salar Pashangzadeh Nazanin Mojtabavi Nazanin Mojtabavi Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis
description	BackgroundGender-related factors have explained the higher prevalence of autoimmune diseases in women. Sex hormones play a key role in the immune system and parenchymal cells function; therefore, these hormones can be important in the pathogenesis of autoimmune diseases as a risk or beneficial factor. Lung fibrosis is the main cause of mortality in systemic sclerosis, a female predominant autoimmune disease. The objective of this study was to examine the effect of progesterone on lung fibrosis in a mouse model of systemic sclerosis.MethodsMice with bleomycin-induced lung fibrosis treated with progesterone subcutaneously for 21 and 28 days. Blood was collected for hormone and cytokine measurement at the end of treatment then, skin and lung tissues were harvested for histological assessment, gene expression, cytokine, hydroxyproline, and gelatinase measurement.ResultsTrichrome staining and hydroxyproline measurements showed that progesterone treatment increased the content of collagen in fibrotic and normal lung tissues. Progesterone increased α-SMA (P < 0.01), TGF- β (P < 0.05) and decreased MMP9 (P < 0.05) in fibrotic lung tissues. Also progesterone treatment decreased the gene expression of Col1a2 (P <0.05), Ctgf (P <01), End1 (0.001) in bleomycin- injured lung tissues. The serum level of TNF-α was decreased, but the serum level of cortisol was increased by progesterone treatment in fibrotic mice (P< 0.05).ConclusionOur results showed that progesterone aggravates lung fibrosis in a mouse model of systemic sclerosis.
format	article
author	Fatemeh Vafashoar Fatemeh Vafashoar Kazem Mousavizadeh Hadi Poormoghim Amir Haghighi Salar Pashangzadeh Salar Pashangzadeh Nazanin Mojtabavi Nazanin Mojtabavi
author_facet	Fatemeh Vafashoar Fatemeh Vafashoar Kazem Mousavizadeh Hadi Poormoghim Amir Haghighi Salar Pashangzadeh Salar Pashangzadeh Nazanin Mojtabavi Nazanin Mojtabavi
author_sort	Fatemeh Vafashoar
title	Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis
title_short	Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis
title_full	Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis
title_fullStr	Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis
title_full_unstemmed	Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis
title_sort	progesterone aggravates lung fibrosis in a mouse model of systemic sclerosis
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/d3bf2047cca3459596c626d0437b4247
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Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis

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