The Role of Progesterone in Cellular Apoptosis of Skin and Lung in a Bleomycin-injured Mouse Model

Vafashoar, Fatemeh; Poormoghim, Hadi; Mousavizadeh, Kazem; Shabestari, Tahereh Mousavi; Tavasoli, Abbas; Javad-Moosavi, Seyed Ali; Mojtabavi, Nazanin

doi:10.18502/ijaai.v18i1.635

Cited by 4 publications

(13 citation statements)

References 38 publications

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“…In contrast, Th2 cells increased collagen accumulation in tissues and inhibited MMPs through IL-4 and IL-13 [3,16]. In our observation, bleomycin injection damages cells in the lung tissue and causes injury, apoptosis, and cellular trafficking in airways, which manages milieu for the occurrence of the fibrosis as mentioned above scenario [10].…”

Section: Discussionsupporting

confidence: 53%

“…Mice were kept in the standard laboratory cages at room temperature and ambient humidity under a 12-hour reverse lightdark cycle. They received ad libitum access to the standard laboratory chow and water [10]. All animal experiments were done according to arrived guideline and were approved by the animal and ethics committee of Iran University of medical sciences (1393.033025094).…”

Section: Animalsmentioning

confidence: 99%

“…PG induces the polarization of M2-type macrophages while it inhibits the functions of M1-type (classically activated) macrophages, e.g., the suppression of TNF-α production [9]. Due to the modulatory effect of PG on inflammation, we established a murine model of scleroderma, and investigate the effect of PG on the cellularity of BAL in SSc mice [10].…”

Section: Introductionmentioning

confidence: 99%

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Progesterone Decreased Cell Infiltration in Airways of Systemic Sclerosis Mice Model

Vafashoar¹,

Mousavizadeh²,

Poormoghim³

et al. 2020

RGM

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Systemic sclerosis (SSc) is the fibrotic autoimmune disease with a higher incidence in women. Lung fibrosis is the most common cause of death in SSc patients. Sex steroids have crucial role in the induction of autoimmune diseases. Progesterone impacts autoimmunity by direct action on parenchymal cells or through its immunomodulatory effect. This study aimed to investigate the effect of progesterone on the cellularity of airways in an animal model of systemic sclerosis. 6 groups of mice were considered in this study. Systemic sclerosis (SSc) was induced in female BALB/c mice by subcutaneous injection of bleomycin for 28 days. For evaluating the effect of Progesterone in SSc model, Progesterone was administered subcutaneously parallel with bleomycin for 28 days or one week after the first administration of bleomycin for 21 days. Further, three control groups were included in this study. On day 29, under lethal anesthesia bronchoalveolar lavage (BAL) was collected and evaluated for cellularity. Our results indicate the increment of cells in BAL of SSc (P<0.0001) mice. Administration of Progesterone for 28 days significantly reduced the infiltrating cells in BALs (P<0.01) of SSc mice. The differential count of BALs indicates that Progesterone reduced the number of lymphocytes (P˂0.05) in SSc mice but did not affect the number of macrophages. Therefore, we conclude that progesterone reduced the inflammatory cells in airways by decreasing the number of lymphocytes.

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Section: Discussionsupporting

confidence: 53%

Section: Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Progesterone Decreased Cell Infiltration in Airways of Systemic Sclerosis Mice Model

Vafashoar¹,

Mousavizadeh²,

Poormoghim³

et al. 2020

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“…Bleomycin injection caused fibrosis in skin and lung tissues of mice as we described in our previous work. 15 Fibrosis was accompanied with an increase in dermis thickness and hydroxyproline amount in skin and lung tissues of mice. 15 Bleomycin injection enhanced the expression of α-SMA in skin and lung tissues of mice compared with control group (p<0.05 in the skin and p<0.001 in the lung) ( Figure 1A, B, C).…”

Section: Bleomycin-induces Fibrosis In Skin and Lung Tissues Of Micementioning

confidence: 99%

“…The dermis thickness was defined as the distance between the epidermal-dermal junction and the dermal-subcutaneous fat junction. 15 After image acquisition from trichrome sections under the light microscope at 100X magnification, the thickness was measured by ImageJ software (Fiji-Win64) in 5 different skin field of each specimen. 15 Tissue microscopic evaluations were performed by two independent observers.…”

Section: Tissue Harvesting Histology and Immunohistochemistrymentioning

confidence: 99%

Gelatinases Increase in Bleomycin-induced Systemic Sclerosis Mouse Model

Vafashoar

Mousavizadeh

Poormoghim

et al. 2019

IJAAI

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Systemic sclerosis is a fibrotic autoimmune disease in which aberrant remodeling of the extracellular matrix in organs disturbs their functionalities. The aim of this study was to investigate the expression of gelatinases on systemic sclerosis. Consequently, a mouse model of systemic sclerosis was employed and the gelatinolytic activity of gelatinases was evaluated on the fibrotic tissues of this model. Two groups of ten mice were considered in this work: a group of systemic sclerosis model and control group. For the generation of systemic sclerosis model, mice received bleomycin, while the control group was subjected to phosphate buffered saline (PBS) reception. Mice were tested for fibrosis by using trichrome staining, hydroxyproline measurement and α-SMA detection in tissue sections. Additionally, the gelatinolytic activity of matrix metalloproteinase 2 and matrix metalloproteinase 9 were measured using gelatin zymography in lungs and skin tissue homogenates. The obtained results indicated that subcutaneous injection of bleomycin-induced fibrosis in skin and lung tissues of mice. Pro and active forms of matrix methaloproteinase 9 were increased in fibrotic lung tissues (p<0.05 and p<0.01, respectively), while, the gelatinolytic activity of MMP2 was unaffected in these tissues. Additionally, in skin tissues of bleomycin-treated animals, both pro and active forms of MMP9 and MMP2 were increased (p<0.05). Pro and active forms of gelatinases increase differently in skin and lung tissues of bleomycin-induced scleroderma.

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Higher fibrotic content of endometriotic lesions is associated with diminished prostaglandin E2 signaling

Huang

Liu

Guo

2021

Reprod Medicine & Biology

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Purpose While the prevailing view holds that the prostaglandin E2 (PGE 2 ) signaling plays a vital role in endometriosis, PGE 2 also is known to be anti‐fibrotic. We investigated the immunostaining of COX‐2, EP2, and EP4, along with fibrotic content in ovarian endometrioma (OE) and deep endometriosis (DE) lesions, and in OE lesions from adolescent and adult patients. In addition, we evaluated the effect of substrate stiffness on the expression of COX‐2, EP2, and EP4 in endometrial stromal cells. Methods Immunohistochemistry analysis of COX‐2, EP2, and EP4, along with the quantification of lesional fibrosis, was conducted for OE and DE lesion samples and also OE lesion samples from adolescent and adult patients. The effect of substrate rigidity on fibroblast‐to‐myofibroblast transdifferentiation (FMT) and the expression of COX‐2, EP2, and EP4, with or without TGF‐β1 stimulation, were investigated. Results The immunostaining of COX‐2, EP2, and EP4 was substantially reduced in endometriotic lesions as lesions became more fibrotic. Both TGF‐β1 stimulation and stiff substrates induced FMT and reduced the expression of COX‐2, EP2, and EP4. Conclusions Since fibrosis is a common feature of endometriosis, our results thus cast doubts on the use of therapeutics that suppresses the PGE 2 signaling pathway, either by inhibiting COX‐2 or EP2/EP4.

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The Role of Progesterone in Cellular Apoptosis of Skin and Lung in a Bleomycin-injured Mouse Model

Cited by 4 publications

References 38 publications

Progesterone Decreased Cell Infiltration in Airways of Systemic Sclerosis Mice Model

Progesterone Decreased Cell Infiltration in Airways of Systemic Sclerosis Mice Model

Gelatinases Increase in Bleomycin-induced Systemic Sclerosis Mouse Model

Higher fibrotic content of endometriotic lesions is associated with diminished prostaglandin E2 signaling

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