scholarly journals Prolactin and vitiligo: proposed autocrine/paracrine actions

2021 ◽  
Vol 18 (1) ◽  
pp. 61
Author(s):  
HebaA Abdelkader ◽  
GhadaM El-Hanafy ◽  
OlfatG Shaker ◽  
Aya Ihab
Keyword(s):  
Paracrine Actions

scholarly journals Betatrophin knockdown induces beiging and mitochondria biogenesis of white adipocytes

2020 ◽  
Vol 245 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Zhe-Zhen Liao ◽  
Xiao-Yan Qi ◽  
Ya-Di Wang ◽  
Jiao-Yang Li ◽  
Qian-Qian Gu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Ampk Signaling ◽  
White Adipocytes ◽  
Beige Adipocytes ◽  
Beige Fat ◽  
Mitochondria Biogenesis ◽  
Paracrine Actions ◽  
White Fat

Remodeling of energy-storing white fat into energy-consuming beige fat has led to a promising new approach to alleviate adiposity. Several studies have shown adipokines can induce white adipose tissue (WAT) beiging through autocrine or paracrine actions. Betatrophin, a novel adipokine, has been linked to energy expenditure and lipolysis but not clearly clarified. Here, we using high-fat diet-induced obesity to determine how betatrophin modulate beiging and adiposity. We found that betatrophin-knockdown mice displayed less white fat mass and decreased plasma TG and NEFA levels. Consistently, inhibition of betatrophin leads to the phenotype change of adipocytes characterized by increased mitochondria contents, beige adipocytes and mitochondria biogenesis-specific markers both in vivo and in vitro. Of note, blocking AMP-activated protein kinase (AMPK) signaling pathway is able to abolish enhanced beige-like characteristics in betatrophin-knockdown adipocytes. Collectively, downregulation of betatrophin induces beiging in white adipocytes through activation of AMPK signaling pathway. These processes suggest betatrophin as a latent therapeutic target for obesity.

scholarly journals Endothelial cells produce bone morphogenetic protein 6 required for iron homeostasis in mice

Blood ◽  
2017 ◽  
Vol 129 (4) ◽  
pp. 405-414 ◽  
Author(s):  
Susanna Canali ◽  
Kimberly B. Zumbrennen-Bullough ◽  
Amanda B. Core ◽  
Chia-Yu Wang ◽  
Manfred Nairz ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Bone Morphogenetic Protein ◽  
Knockout Mice ◽  
Iron Homeostasis ◽  
Conditional Knockout ◽  
Conditional Knockout Mice ◽  
Morphogenetic Protein ◽  
Key Points ◽  
Paracrine Actions ◽  
Bone Morphogenetic Protein 6

Key Points Endothelial Bmp6 conditional knockout mice exhibit hemochromatosis, whereas hepatocyte and macrophage Bmp6 conditional knockout mice do not. Our data support a model in which EC Bmp6 has paracrine actions on hepatocyte hemojuvelin to regulate hepcidin production.

Stem cell paracrine actions in tissue regeneration and potential therapeutic effect in human endometrium: a retrospective study

2020 ◽  
Vol 127 (5) ◽  
pp. 551-560 ◽  
Author(s):  
L Miguel‐Gómez ◽  
H Ferrero ◽  
S López‐Martínez ◽  
H Campo ◽  
N López‐Pérez ◽  
...  
Keyword(s):  
Stem Cell ◽  
Retrospective Study ◽  
Therapeutic Effect ◽  
Tissue Regeneration ◽  
Human Endometrium ◽  
Paracrine Actions

scholarly journals Systematic Exposition of Mesenchymal Stem Cell for Inflammatory Bowel Disease and Its Associated Colorectal Cancer

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Jingjing Kang ◽  
Li Zhang ◽  
Xiao Luo ◽  
Xiangyu Ma ◽  
Gaoying Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Research Progress ◽  
Cell Contact ◽  
Wide Range ◽  
Therapeutic Mechanism ◽  
Inflammatory Bowel ◽  
Paracrine Actions ◽  
Different Sources

Mesenchymal stem cells (MSCs) therapy has been applied to a wide range of diseases with excessive immune response, including inflammatory bowel disease (IBD), owing to its powerful immunosuppression and its ability to repair tissue lesions. Different sources of MSCs show different therapeutic properties. Engineering managements are able to enhance the immunomodulation function and the survival of MSCs involved in IBD. The therapeutic mechanism of MSCs in IBD mainly focuses on cell-to-cell contact and paracrine actions. One of the promising therapeutic options for IBD can focus on exosomes of MSCs. MSCs hold promise for the treatment of IBD-associated colorectal cancer because of their tumor-homing function and chronic inflammation inhibition. Encouraging results have been obtained from clinical trials in IBD and potential challenges caused by MSCs therapy are getting solved. This review can assist investigators better to understand the research progress for enhancing the efficacy of MSCs therapy involved in IBD and CAC.

Bone marrow mesenchymal stem cells promote the repair of islets from diabetic mice through paracrine actions

2014 ◽  
Vol 388 (1-2) ◽  
pp. 41-50 ◽  
Author(s):  
Xiaodong Gao ◽  
Lujun Song ◽  
Kuntang Shen ◽  
Hongshan Wang ◽  
Mengjia Qian ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Diabetic Mice ◽  
Marrow Mesenchymal Stem Cells ◽  
Paracrine Actions

Atrial and pulmonary endothelin mRNA is increased in a canine model of chronic low cardiac output

1997 ◽  
Vol 273 (2) ◽  
pp. R838-R844 ◽  
Author(s):  
C. M. Wei ◽  
A. L. Clavell ◽  
J. C. Burnett
Keyword(s):  
Cardiac Output ◽  
Immunohistochemical Staining ◽  
Canine Model ◽  
Pulmonary Tissue ◽  
Low Cardiac Output ◽  
Inferior Vena Caval ◽  
Pulmonary Epithelial Cells ◽  
Key Sites ◽  
Potent Vasoconstrictor ◽  
Paracrine Actions

Chronic thoracic inferior vena caval constriction (TIVCC) is a model of low-cardiac output congestive heart failure (CHF), in which pulmonary and atrial as well as circulating endothelin (ET) are increased. ET is a potent vasoconstrictor and mitogenic peptide whose circulating concentrations are increased in severe human and experimental CHF. To date, an increase in ET production at key sites in CHF remains controversial. Therefore, the current study was designed to determine cardiac and pulmonary ET-1 mRNA in an experimental model of CHF produced by TIVCC in which avid sodium retention, intense vasoconstriction, and elevation of circulating ET-1 occur as in human CHF. Experiments were conducted in normal dogs and dogs with 7 days of TIVCC. Cardiac and pulmonary ET-1 mRNA were measured by quantified densitometry of Northern blots. Plasma and tissue (cardiac and pulmonary) ET-1 immunoreactivity were determined by radioimmunoassay. Cardiac and pulmonary tissue localization of ET-1 were determined by immunohistochemical staining. Plasma ET-1 was significantly increased in TIVCC compared with normal dogs. ET-1 mRNA was detectable in normal canine atria, ventricle, and lung. ET-1 mRNA was significantly increased in TIVCC compared with normal dogs in both atrial and pulmonary tissues without alternations in ventricular ET mRNA. Atrial and pulmonary tissue concentrations of ET-1 also were markedly elevated in TIVCC compared with normal dogs. Immunohistochemical staining of atrial and pulmonary tissues for ET-1 demonstrated that the increased ET immunoreactivity was localized to atrial myocytes and pulmonary epithelial cells. These studies support a role for the heart and lung in the increased production of ET-1 in CHF. The current studies also suggest that ET-1 may have important autocrine and paracrine actions in cardiopulmonary regulation in experimental CHF.

scholarly journals The exosome-mediated autocrine and paracrine actions of plasma gelsolin in ovarian cancer chemoresistance

Oncogene ◽  
2019 ◽  
Vol 39 (7) ◽  
pp. 1600-1616 ◽  
Author(s):  
Meshach Asare-Werehene ◽  
Kiran Nakka ◽  
Arkadiy Reunov ◽  
Chen-Tzu Chiu ◽  
Wei-Ting Lee ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Fate ◽  
Gynecological Cancer ◽  
Late Presentation ◽  
High Recurrence Rate ◽  
Free Survival ◽  
Plasma Gelsolin ◽  
Elevated Expression ◽  
Paracrine Actions ◽  
Cancer Chemoresistance

Abstract Ovarian cancer (OVCA) is the most lethal gynecological cancer, due predominantly to late presentation, high recurrence rate and common chemoresistance development. The expression of the actin-associated protein cytosolic gelsolin (GSN) regulates the gynecological cancer cell fate resulting in dysregulation in chemosensitivity. In this study, we report that elevated expression of plasma gelsolin (pGSN), a secreted isoform of GSN and expressed from the same GSN gene, correlates with poorer overall survival and relapse-free survival in patients with OVCA. In addition, it is highly expressed and secreted in chemoresistant OVCA cells than its chemosensitive counterparts. pGSN, secreted and transported via exosomes (Ex-pGSN), upregulates HIF1α–mediated pGSN expression in chemoresistant OVCA cells in an autocrine manner as well as confers cisplatin resistance in otherwise chemosensitive OVCA cells. These findings support our hypothesis that exosomal pGSN promotes OVCA cell survival through both autocrine and paracrine mechanisms that transform chemosensitive cells to resistant counterparts. Specifically, pGSN transported via exosomes is a determinant of chemoresistance in OVCA.

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