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Recent Advances in the Pathobiology of Diabetes Mellitus and Its Complications

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 5494

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Special Issue Editor

Prof. Dr. Das Undurti

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Guest Editor

UND Life Sciences, 2221 NW 5th St., Battle Ground, WA 98604, USA
Interests: essential fatty acids; eicosanoids; cytokines; free radicals; nitric oxide; melatonin and their role in various clinical conditions

Special Issue Information

Dear Colleagues,

Several diseases, including cancer, radiation-induced damage and its usefulness in cancer therapy, metabolic syndrome (inclduing obesity, diabetes mellitus, hypertension, cadiovascular diseases), Alzheimer‘ disease, COVID-19 infection and its complications suchas ARDS, sepsis, multiple sclerosis, and other diseases, all have inflammation and altered immune system as the underlying mechanism(s) in their pathobiology and hence the keys to their prevention and management. The various factors involved in inflamamtory events and immune system dysregulation in thsese diseases include altered cytokines, reactive oxygen species, adhesion factors, T and B cell dysregulation, lipid mediators, changes in genes/oncogenes expression, cytoskeleton abnormalities, etc. Hence, it is important to understand how all these events/factors interact with each other and what these interaction(s) mean for various physiological and pathological processes and diseases. This implies that we need to develop a comprehensive understanding of various cellular events and processes pertaining to inflammation, anti-inflammation, immune response and its regulation and dysregulation, wound healing, and the restoration of homeostasis. This Special Issue focusses on such events and cellular processes. We coordially invite all scientists/physicians/cell biologists and others who wish to develop a comprehensive view of physiology and pathology in a wholesome manner. Based on the development of such concepts, we anticipate and encourage all authors to develop and propose novel preventive and therapeutic approaches to various diseases—no matter how radical or unthinkable they appear to be at present. We particularly encourage authors to propose novel ideas that appear to be against the current dogma(s) (but they need to be logical, reasonable, and convincing) and how such ideas can be verified or tested also have to be suggested for others to test these ideas.

Prof. Dr. Das Undurti
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

physiology
pathology
pathogenesis
cytokines
lipids
cytokines
ROS
genes
oncogenes
epigenetics
cancer
radiation
adhesion molecules
DNA
RNA

Published Papers (3 papers)

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Research

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12 pages, 931 KiB

Open AccessArticle

PLAAT1 Exhibits Phosphatidylcholine:Monolysocardiolipin Transacylase Activity

by Ryan M. Bradley, Ashkan Hashemi, Juan J. Aristizabal-Henao, Ken D. Stark and Robin E. Duncan

Int. J. Mol. Sci. 2022, 23(12), 6714; https://doi.org/10.3390/ijms23126714 - 16 Jun 2022

Cited by 2 | Viewed by 1482

Abstract

Tissue-specific cardiolipin fatty acyl profiles are achieved by remodeling of de novo synthesized cardiolipin, and four remodeling enzymes have thus far been identified. We studied the enzyme phospholipase A and acyltransferase 1 (PLAAT1), and we report the discovery that it has phosphatidylcholine (PC):monolysocardiolipin (MLCL) transacylase activity. Subcellular localization was analyzed by differential centrifugation and immunoblotting. Total levels of major phospholipids, and the fatty acyl profile of cardiolipin, were analyzed in HEK293 cells expressing murine PLAAT1 using gas chromatography. Apparent enzyme kinetics of affinity-purified PLAAT1 were calculated using radiochemical enzyme assays. This enzyme was found to localize predominantly to the endoplasmic reticulum (ER) but was detected at low levels in the mitochondria-associated ER matrix. Cells expressing PLAAT1 had higher levels of total cardiolipin, but not other phospholipids, and it was primarily enriched in the saturated fatty acids myristate, palmitate, and stearate, with quantitatively smaller increases in the n-3 polyunsaturated fatty acids linolenate, eicosatrienoate, and eicosapentanoate and the monounsaturated fatty acid erucate. Affinity-purified PLAAT1 did not catalyze the transacylation of MLCL using 1-palmitoyl-2-[¹⁴C]-linoleoyl-PC as an acyl donor. However, PLAAT1 had an apparent V_max of 1.61 μmol/min/mg protein and Km of 126 μM using [9,10-³H]-distearoyl-PC as an acyl donor, and 0.61 μmol/min/mg protein and Km of 16 μM using [9,10-³H]-dioleoyl-PC. PLAAT1 is therefore a novel PC:MLCL transacylase. Full article

(This article belongs to the Special Issue Recent Advances in the Pathobiology of Diabetes Mellitus and Its Complications)

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13 pages, 1295 KiB

Open AccessArticle

Glucagon-like Peptide-1 Secretion Is Inhibited by Lysophosphatidic Acid

by Maria F. Fernandes, Michelle V. Tomczewski and Robin E. Duncan

Int. J. Mol. Sci. 2022, 23(8), 4163; https://doi.org/10.3390/ijms23084163 - 09 Apr 2022

Cited by 4 | Viewed by 1816

Abstract

Glucagon-like peptide-1 (GLP-1) potentiates glucose-stimulated insulin secretion (GSIS). While dozens of compounds stimulate GLP-1 secretion, few inhibit. Reduced GLP-1 secretion and impaired GSIS occur in chronic inflammation. Lysophosphatidic acids (LPAs) are bioactive phospholipids elevated in inflammation. The aim of this study was to test whether LPA inhibits GLP-1 secretion in vitro and in vivo. GLUTag L-cells were treated with various LPA species, with or without LPA receptor (LPAR) antagonists, and media GLP-1 levels, cellular cyclic AMP and calcium ion concentrations, and DPP4 activity levels were analyzed. Mice were injected with LPA, with or without LPAR antagonists, and serum GLP-1 and DPP4 activity were measured. GLUTag GLP-1 secretion was decreased ~70–90% by various LPAs. GLUTag expression of Lpar1, 2, and 3 was orders of magnitude higher than Lpar4, 5, and 6, implicating the former group in this effect. In agreement, inhibition of GLP-1 secretion was reversed by the LPAR1/3 antagonist Ki16425, the LPAR1 antagonists AM095 and AM966, or the LPAR2 antagonist LPA2-antagonist 1. We hypothesized involvement of Gα_i-mediated LPAR activity, and found that intracellular cyclic AMP and calcium ion concentrations were decreased by LPA, but restored by Ki16425. Mouse LPA injection caused an ~50% fall in circulating GLP-1, although only LPAR1 or LPAR1/3 antagonists, but not LPAR2 antagonism, prevented this. GLUTag L-cell and mouse serum DPP4 activity was unchanged by LPA or LPAR antagonists. LPA therefore impairs GLP-1 secretion in vitro and in vivo through Gα_i-coupled LPAR1/3 signaling, providing a new mechanism linking inflammation with impaired GSIS. Full article

(This article belongs to the Special Issue Recent Advances in the Pathobiology of Diabetes Mellitus and Its Complications)

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Review

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16 pages, 936 KiB

Open AccessReview

Immune Modulation by Myeloid-Derived Suppressor Cells in Diabetic Kidney Disease

by Ching-Chuan Hsieh, Cheng-Chih Chang, Yung-Chien Hsu and Chun-Liang Lin

Int. J. Mol. Sci. 2022, 23(21), 13263; https://doi.org/10.3390/ijms232113263 - 31 Oct 2022

Cited by 4 | Viewed by 1679

Abstract

Diabetic kidney disease (DKD) frequently leads to end-stage renal disease and other life-threatening illnesses. The dysregulation of glomerular cell types, including mesangial cells, endothelial cells, and podocytes, appears to play a vital role in the development of DKD. Myeloid-derived suppressor cells (MDSCs) exhibit immunoregulatory and anti-inflammatory properties through the depletion of L-arginine that is required by T cells, through generation of oxidative stress, interference with T-cell recruitment and viability, proliferation of regulatory T cells, and through the promotion of pro-tumorigenic functions. Under hyperglycemic conditions, mouse mesangial cells reportedly produce higher levels of fibronectin and pro-inflammatory cytokines. Moreover, the number of MDSCs is noticeably decreased, weakening inhibitory immune activities, and creating an inflammatory environment. In diabetic mice, immunotherapy with MDSCs that were induced by a combination of granulocyte-macrophage colony-stimulating factor, interleukin (IL)-1β, and IL-6, reduced kidney to body weight ratio, fibronectin expression, and fibronectin accumulation in renal glomeruli, thus ameliorating DKD. In conclusion, MDSCs exhibit anti-inflammatory activities that help improve renal fibrosis in diabetic mice. The therapeutic targeting of the proliferative or immunomodulatory pathways of MDSCs may represent an alternative immunotherapeutic strategy for DKD. Full article

(This article belongs to the Special Issue Recent Advances in the Pathobiology of Diabetes Mellitus and Its Complications)

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