scholarly journals The Expanding Role of Mitochondria, Autophagy and Lipophagy in Steroidogenesis

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1851
Author(s):  
Geetika Bassi ◽  
Simarjit Kaur Sidhu ◽  
Suresh Mishra
Keyword(s):  
Potential Role ◽  
Cell Types ◽  
Cholesterol Homeostasis ◽  
Cholesterol Transport ◽  
Inner Mitochondrial Membrane ◽  
Mitochondrial Structure ◽  
Steroidogenic Cell ◽  
Start Domain ◽  
Steroidogenic Cells

The fundamental framework of steroidogenesis is similar across steroidogenic cells, especially in initial mitochondrial steps. For instance, the START domain containing protein-mediated cholesterol transport to the mitochondria, and its conversion to pregnenolone by the enzyme P450scc, is conserved across steroidogenic cells. The enzyme P450scc localizes to the inner mitochondrial membrane, which makes the mitochondria essential for steroidogenesis. Despite this commonality, mitochondrial structure, number, and dynamics vary substantially between different steroidogenic cell types, indicating implications beyond pregnenolone biosynthesis. This review aims to focus on the growing roles of mitochondria, autophagy and lipophagy in cholesterol uptake, trafficking and homeostasis in steroidogenic cells and consequently in steroidogenesis. We will focus on these aspects in the context of the physiological need for different steroid hormones and cell-intrinsic inherent features in different steroidogenic cell types beyond mitochondria as a mere site for the beginning of steroidogenesis. The overall goal is to provide an authentic and comprehensive review on the expanding role of steroidogenic cell-intrinsic processes in cholesterol homeostasis and steroidogenesis, and to bring attention to the scientific community working in this field on these promising advancements. Moreover, we will discuss a novel mitochondrial player, prohibitin, and its potential role in steroidogenic mitochondria and cells, and consequently, in steroidogenesis.

scholarly journals Lipid and Cholesterol Homeostasis after Arsenic Exposure and Antibiotic Treatment in Mice: Potential Role of the Microbiota

2019 ◽  
Vol 127 (9) ◽  
pp. 097002 ◽  
Author(s):  
Liang Chi ◽  
Yunjia Lai ◽  
Pengcheng Tu ◽  
Chih-Wei Liu ◽  
Jingchuan Xue ◽  
...  
Keyword(s):  
Antibiotic Treatment ◽  
Potential Role ◽  
Arsenic Exposure ◽  
Cholesterol Homeostasis

scholarly journals Liposomes in tissue engineering and regenerative medicine

2014 ◽  
Vol 11 (101) ◽  
pp. 20140459 ◽  
Author(s):  
Nelson Monteiro ◽  
Albino Martins ◽  
Rui L. Reis ◽  
Nuno M. Neves
Keyword(s):  
Tissue Engineering ◽  
Regenerative Medicine ◽  
Potential Role ◽  
Lipid Membrane ◽  
Cultured Cells ◽  
Cell Types ◽  
Biomaterial Scaffolds ◽  
Bioactive Agents ◽  
The 1960S

Liposomes are vesicular structures made of lipids that are formed in aqueous solutions. Structurally, they resemble the lipid membrane of living cells. Therefore, they have been widely investigated, since the 1960s, as models to study the cell membrane, and as carriers for protection and/or delivery of bioactive agents. They have been used in different areas of research including vaccines, imaging, applications in cosmetics and tissue engineering. Tissue engineering is defined as a strategy for promoting the regeneration of tissues for the human body. This strategy may involve the coordinated application of defined cell types with structured biomaterial scaffolds to produce living structures. To create a new tissue, based on this strategy, a controlled stimulation of cultured cells is needed, through a systematic combination of bioactive agents and mechanical signals. In this review, we highlight the potential role of liposomes as a platform for the sustained and local delivery of bioactive agents for tissue engineering and regenerative medicine approaches.

Sucrose transport and phloem unloading in peach fruit: potential role of two transporters localized in different cell types

2014 ◽  
Vol 154 (2) ◽  
pp. 179-193 ◽  
Author(s):  
Laura Zanon ◽  
Rachele Falchi ◽  
Simonetta Santi ◽  
Giannina Vizzotto
Keyword(s):  
Potential Role ◽  
Cell Types ◽  
Sucrose Transport ◽  
Phloem Unloading ◽  
Peach Fruit ◽  
Different Cell Types

scholarly journals Syntaxin 17 Is Abundant in Steroidogenic Cells and Implicated in Smooth Endoplasmic Reticulum Membrane Dynamics

2000 ◽  
Vol 11 (8) ◽  
pp. 2719-2731 ◽  
Author(s):  
Martin Steegmaier ◽  
Viola Oorschot ◽  
Judith Klumperman ◽  
Richard H. Scheller
Keyword(s):  
Endoplasmic Reticulum ◽  
Smooth Endoplasmic Reticulum ◽  
Regulatory Protein ◽  
Cell Types ◽  
Membrane Dynamics ◽  
Endoplasmic Reticulum Membrane ◽  
Steroidogenic Cell ◽  
Molecular Machinery ◽  
Intermediate Compartment ◽  
Steroidogenic Cells

The endoplasmic reticulum (ER) consists of subcompartments that have distinct protein constituents, morphological appearances, and functions. To understand the mechanisms that regulate the intricate and dynamic organization of the endoplasmic reticulum, it is important to identify and characterize the molecular machinery involved in the assembly and maintenance of the different subcompartments. Here we report that syntaxin 17 is abundantly expressed in steroidogenic cell types and specifically localizes to smooth membranes of the ER. By immunoprecipitation analyses, syntaxin 17 exists in complexes with a syntaxin regulatory protein, rsly1, and/or two intermediate compartment SNARE proteins, rsec22b and rbet1. Furthermore, we found that syntaxin 17 is anchored to the smooth endoplasmic reticulum through an unusual mechanism, requiring two adjacent hydrophobic domains near its carboxyl terminus. Converging lines of evidence indicate that syntaxin 17 functions in a vesicle-trafficking step to the smooth-surfaced tubular ER membranes that are abundant in steroidogenic cells.

scholarly journals Factor XIII Subunit A in the Skin: Applications in Diagnosis and Treatment

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Lilla Paragh ◽  
Daniel Törőcsik
Keyword(s):  
Factor Xiii ◽  
Potential Role ◽  
Cell Types ◽  
Subunit A ◽  
Therapeutic Implications ◽  
Inflammatory Conditions ◽  
Dermal Cell ◽  
Wide Range

The role of factor XIII subunit A (FXIII-A) is not restricted to hemostasis. FXIII-A is also present intracellularly in several human cells and serves as a diagnostic marker in a wide range of dermatological diseases from inflammatory conditions to malignancies. In this review, we provide a guide on the still controversial interpretation of dermal cell types expressing FXIII-A and assess the previously described mechanisms behind their accumulation under physiological and pathological conditions of the human skin. We summarize the intracellular functions of FXIII-A as well as its possible sources in the extracellular space of the dermis with a focus on its relevance to skin homeostasis and disease pathogenesis. Finally, the potential role of FXIII-A in wound healing, as a field with long-term therapeutic implications, is also discussed.

scholarly journals Regulation of adrenal and ovarian steroidogenesis by miR-132

2017 ◽  
Vol 59 (3) ◽  
pp. 269-283 ◽  
Author(s):  
Zhigang Hu ◽  
Wen-Jun Shen ◽  
Fredric B Kraemer ◽  
Salman Azhar
Keyword(s):  
Target Gene ◽  
Potential Role ◽  
Gene Products ◽  
Adrenal Cells ◽  
Mecp2 Protein ◽  
Direct Target ◽  
Steroidogenic Cells ◽  
And Function ◽  
Camp Stimulation

miR-132 is hormonally regulated in steroidogenic cells of the adrenal gland, ovary and testis. Here, we examined the potential role of miR-132 in the control of steroidogenesis. Transfection of Y1 adrenal cells with miR-132 increased mRNAs of 3β-HSD and 20α-HSD enzymes, which catalyze the sequential conversion of pregnenolone to progesterone to biologically inactive 20α-hydroxyprogesterone (20α-OHP). Overexpression of miR-132 reduced MeCP2 and StAR protein expression, basal progestin (progesterone and 20α-OHP) production, but enhanced their production in response to cAMP stimulation. Use of [3H] pregnenolone and free-diffusible 22(R)-hydroxycholesterol further confirmed that miR-132 promotes the production of 20α-OHP by upregulating 3β-HSD and 20α-HSD. Evidence is also presented that StAR is a direct target of miR-132. Transient transfection of Y1 cells with miR-132 demonstrated that miR-132 induction of 3β-HSD and 20α-HSD was accompanied by significant suppression of one of its target gene products, MeCP2. In contrast, co-expression of miR-132 plus MeCP2 protein partially blocked the ability of miR-132 to upregulate the expression and function of 3β-HSD and 20α-HSD. Moreover, suppression of MeCP2 protein with siRNA resulted in increased expression of 3β-HSD and 20α-HSD, further demonstrating that miR-132 induces the expression of these two enzymes via inhibition of MeCP2. Likewise, overexpression of miR-132 increased 20α-OHP production with and without HDL loading, while knockdown of miR-132 resulted in a significant decrease of 20α-OHP production by granulosa cells. In conclusion, our data suggest that miR-132 attenuates steroidogenesis by repressing StAR expression and inducing 20α-HSD via inhibition of MeCP2 to generate a biologically inactive 20α-OHP.

scholarly journals Iron Overload, Oxidative Stress, and Ferroptosis in the Failing Heart and Liver

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1864
Author(s):  
Daniele Mancardi ◽  
Mariarosa Mezzanotte ◽  
Elisa Arrigo ◽  
Alice Barinotti ◽  
Antonella Roetto
Keyword(s):  
Cell Death ◽  
Iron Overload ◽  
Redox Homeostasis ◽  
Cell Types ◽  
Iron Accumulation ◽  
Oxygen Species ◽  
Hepatic Inflammation ◽  
Mitochondrial Structure ◽  
Different Cell Types

Iron accumulation is a key mediator of several cytotoxic mechanisms leading to the impairment of redox homeostasis and cellular death. Iron overload is often associated with haematological diseases which require regular blood transfusion/phlebotomy, and it represents a common complication in thalassaemic patients. Major damages predominantly occur in the liver and the heart, leading to a specific form of cell death recently named ferroptosis. Different from apoptosis, necrosis, and autophagy, ferroptosis is strictly dependent on iron and reactive oxygen species, with a dysregulation of mitochondrial structure/function. Susceptibility to ferroptosis is dependent on intracellular antioxidant capacity and varies according to the different cell types. Chemotherapy-induced cardiotoxicity has been proven to be mediated predominantly by iron accumulation and ferroptosis, whereas there is evidence about the role of ferritin in protecting cardiomyocytes from ferroptosis and consequent heart failure. Another paradigmatic organ for transfusion-associated complication due to iron overload is the liver, in which the role of ferroptosis is yet to be elucidated. Some studies report a role of ferroptosis in the initiation of hepatic inflammation processes while others provide evidence about an involvement in several pathologies including immune-related hepatitis and acute liver failure. In this manuscript, we aim to review the literature to address putative common features between the response to ferroptosis in the heart and liver. A better comprehension of (dys)similarities is pivotal for the development of future therapeutic strategies that can be designed to specifically target this type of cell death in an attempt to minimize iron-overload effects in specific organs.

scholarly journals IL-22 is involved in liver regeneration after hepatectomy

2010 ◽  
Vol 298 (1) ◽  
pp. G74-G80 ◽  
Author(s):  
Xiaodan Ren ◽  
Bin Hu ◽  
Lisa M. Colletti
Keyword(s):  
Liver Regeneration ◽  
General Anesthesia ◽  
Partial Hepatectomy ◽  
Potential Role ◽  
Cellular Proliferation ◽  
Cell Types ◽  
In Vitro Studies ◽  
Hepatocyte Proliferation

Hepatocyte proliferation following partial hepatectomy is an important component of liver regeneration, and recent in vitro studies have shown that IL-22 is involved in cellular proliferation in a variety of cell types, including hepatocytes. IL-22 functions through IL-10Rβ and IL-22Rα. The goal of this study was to investigate the potential role of IL-22 in liver regeneration after 70% hepatectomy. Following 70% hepatectomy, done under general anesthesia in mice, serum IL-22 and hepatic IL-22Rα mRNA were significantly increased. Although administration of exogenous IL-22 prior to hepatectomy did not increase hepatocyte proliferation, administration of anti-IL-22 antibody before hepatectomy did significantly decrease hepatocyte proliferation. Furthermore, IL-22 treatment prior to 70% hepatectomy induced stat-3 activation; no significant changes were seen in ERK1/2 activation, stat-1 activation, or stat-5 activation. IL-22 pretreatment also significantly increased hepatic and serum IL-6 levels. In addition, animals treated with anti-IL-22 antibody also expressed less TGF-α. In conclusion, these data suggest that IL-22 is involved in liver regeneration and this may be due to interaction with IL-6 and TGF-α cascades.

scholarly journals Lovastatin fails to improve motor performance and survival in methyl-CpG-binding protein2-null mice

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Claudia Villani ◽  
Giuseppina Sacchetti ◽  
Renzo Bagnati ◽  
Alice Passoni ◽  
Federica Fusco ◽  
...  
Keyword(s):  
Rett Syndrome ◽  
Potential Role ◽  
Cholesterol Metabolism ◽  
Cholesterol Homeostasis ◽  
Motor Deficits ◽  
Brain Cholesterol ◽  
Background Strain ◽  
Cholesterol Levels ◽  
The Brain

Previous studies provided evidence for the alteration of brain cholesterol homeostasis in 129.Mecp2-null mice, an experimental model of Rett syndrome. The efficacy of statins in improving motor symptoms and prolonging survival of mutant mice suggested a potential role of statins in the therapy of Rett syndrome. In the present study, we show that Mecp2 deletion had no effect on brain and reduced serum cholesterol levels and lovastatin (1.5 mg/kg, twice weekly as in the previous study) had no effects on motor deficits and survival when Mecp2 deletion was expressed on a background strain (C57BL/6J; B6) differing from that used in the earlier study. These findings indicate that the effects of statins may be background specific and raise important issues to consider when contemplating clinical trials. The reduction of the brain cholesterol metabolite 24S-hydroxycholesterol (24S-OHC) found in B6.Mecp2-null mice suggests the occurrence of changes in brain cholesterol metabolism and the potential utility of using plasma levels of 24S-OHC as a biomarker of brain cholesterol homeostasis in RTT.

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