LincRNA-EPS Promotes Proliferation of Aged Dermal Fibroblast by Inducing CCND1.

The aging process is linked to numerous cellular changes, among which are modifications in the functionality of dermal fibroblasts. These fibroblasts play a crucial role in sustaining the healing of skin wounds. Reduced cell proliferation is a hallmark feature of aged dermal fibroblasts.

miR-146a Decreases Inflammation and ROS Production in Aged Dermal Fibroblasts.

Aging is associated with a decline in the functionality of various cell types, including dermal fibroblasts, which play a crucial role in maintaining skin homeostasis and wound healing. Chronic inflammation and increased reactive oxygen species (ROS) production are hallmark features of aging, contributing to impaired wound healing. MicroRNA-146a (miR-146a) has been implicated as a critical regulator of inflammation and oxidative stress in different cell types, yet its role in aged dermal fibroblasts and its potential relevance to wound healing remains poorly understood.

Predictive Accuracy Comparison of Prognostic Scoring Systems for Survival in Patients Undergoing TIPS Placement: A Systematic Review and Meta-analysis.

Rationale And Objectives: This meta-analysis aimed to evaluate the performance of different risk assessment models (RAMs) for survival after Transjugular Intrahepatic Portosystemic Shunt (TIPS) in patients with cirrhotic portal hypertension.

Materials And Methods: A systematic search of PubMed, WOS, Embase, Cochrane, and CNKI from inception to February 2023 was conducted. We comprehensively reviewed and aggregated data from numerous studies covering prevalent RAMs such as Child-Turcotte-Pugh, the Model for End-Stage Liver Disease (MELD), MELD-Sodium (MELD-Na), the Freiburg Index of Post-TIPS Survival (FIPS), Bilirubin-platelet, Chronic Liver Failure Consortium Acute Decompensation score, and Albumin-Bilirubin grade across different timeframes.

Triazolothiadiazine derivative positively modulates CXCR4 signaling and improves diabetic wound healing.

Development of specific therapies that target and accelerate diabetic wound repair is an urgent need to alleviate pain and suffering and the huge socioeconomic burden of this debilitating disease. C-X-C Motif Chemokine Ligand 12 (CXCL12) also know an stromal cell-derived factor 1α (SDF-1α) is a chemokine that binds the CXC chemokine receptor type 4 (CXCR4) and activates downstream signaling resulting in recruitment of hematopoietic cells to locations of tissue injury and promotes tissue repair. In diabetes, low expression of CXCL12 correlates with impaired wound healing.

LncRNA MALAT1 Regulates Hyperglycemia Induced EMT in Keratinocyte via miR-205.

Epithelial-to-mesenchymal transition (EMT) is critical to cutaneous wound healing. When skin is injured, EMT activates and mobilizes keratinocytes toward the wound bed, therefore enabling re-epithelialization. This process becomes dysregulated in patients with diabetes mellitus (DM).

Discovery of Small Molecule Activators of Chemokine Receptor CXCR4 That Improve Diabetic Wound Healing.

Diabetes produces a chronic inflammatory state that contributes to the development of vascular disease and impaired wound healing. Despite the known individual and societal impacts of diabetic ulcers, there are limited therapies effective at improving healing. Stromal cell-derived factor 1α (SDF-1α) is a CXC chemokine that functions via activation of the CXC chemokine receptor type 4 (CXCR4) receptor to recruit hematopoietic cells to locations of tissue injury and promote tissue repair.

LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte.

One of the major complications in diabetes is impaired wound healing. Unfortunately, effective therapies are currently lacking. Epithelial to mesenchymal transition (EMT) is a critical process involved in cutaneous wound healing.

Cerium oxide nanoparticle delivery of microRNA-146a for local treatment of acute lung injury.

Acute respiratory distress syndrome (ARDS) is a devastating pulmonary disease with significant in-hospital mortality and is the leading cause of death in COVID-19 patients. Excessive leukocyte recruitment, unregulated inflammation, and resultant fibrosis contribute to poor ARDS outcomes. Nanoparticle technology with cerium oxide nanoparticles (CNP) offers a mechanism by which unstable therapeutics such as the anti-inflammatory microRNA-146a can be locally delivered to the injured lung without systemic uptake.

Deviations in MicroRNA-21 Expression Patterns Identify a Therapeutic Target for Diabetic Wound Healing.

Chronic inflammation plays a major role in impaired healing of diabetic wounds. Mounting evidence highlights the role of controlled, sequential polarization of macrophages in producing the appropriate progression through the stages of wound healing: inflammation (pro- inflammatory stage), proliferation and remodeling (regenerative stage). Non-coding RNAs, including microRNAs, maintain critical roles in regulating normal biological processes, such as wound healing; and are being explored as therapeutic targets for modulating dysfunction in disease states.

Upregulation of long noncoding RNA growth arrest-specific 5 mediates pro-inflammatory mechanisms of diabetic wound healing impairment.

Unresolved inflammatory processes contribute to impaired healing in diabetic wounds, with increasing evidence implicating persistent pro-inflammatory macrophage polarization as a driver of chronic inflammation and delayed wound closure. Previous investigations aimed to uncover the role of regulatory RNAs in macrophage polarization and to understand how aberrant expression patterns contribute to wound healing impairment, with the goal of identifying novel therapeutic targets for promoting normal wound healing progression. In the Journal of Investigative Dermatology, Hu et al.

Nanosilk Increases the Strength of Diabetic Skin and Delivers CNP-miR146a to Improve Wound Healing.

Diabetes mellitus is a metabolic disorder associated with properties and an increased risk of chronic wounds due to sustained pro-inflammatory response. We have previously of radical scavenging cerium oxide nanoparticles (CNP) conjugated to the anti-inflammatory microRNA (miR)-146a, termed CNP-miR146a, improves diabetic wound healing by synergistically lowering oxidative stress and inflammation, and we sought to evaluate this treatment in a topical application. Silk fibroin is a biocompatible polymer that can be fabricated into nanostructures, termed nanosilk.

Role of microRNA-21 and Its Underlying Mechanisms in Inflammatory Responses in Diabetic Wounds.

A central feature of diabetic wounds is the persistence of chronic inflammation, which is partly due to the prolonged presence of pro-inflammatory (M1) macrophages in diabetic wounds. Persistence of the M1 macrophage phenotype and failure to transition to the regenerative or pro-remodeling (M2) macrophage phenotype plays an indispensable role in diabetic wound impairment; however, the mechanism underlying this relationship remains unclear. Recently, microRNAs have been shown to provide an additional layer of regulation of gene expression.

Long Noncoding RNA GAS5 Regulates Macrophage Polarization and Diabetic Wound Healing.

A central feature of diabetic (Db) wounds is the persistence of chronic inflammation, which is partly due to the prolonged presence of proinflammatory (M1) macrophages. Using in vivo and in vitro analyses, we have tested the hypothesis that long noncoding RNA GAS5 is dysregulated in Db wounds. We have assessed the contribution of GAS5 to the M1 macrophage phenotype, as well as the functional consequences of knocking down its expression.

Mesenchymal stromal cells contract collagen more efficiently than dermal fibroblasts: Implications for cytotherapy.

Background: Stem cell therapy is the next generation a well-established technique. Cell therapy with mesenchymal stem cells (MSC) has been demonstrated to enhance wound healing in diabetic mice, at least partly due to improved growth factor production. However, it is unclear whether MSC can biomechanically affect wound closure.

Differential Expression of Transforming Growth Factor-β1 Is Associated With Fetal Regeneration After Myocardial Infarction.

Background: Global extracellular matrix (ECM)-related gene expression is decreased after myocardial infarction (MI) in fetal sheep when compared with adult sheep. Transforming growth factor (TGF)-β1 is a key regulator of ECM; therefore we hypothesize that TGF-β1 is differentially expressed in adult and fetal infarcts after MI.

Methods: Adult and fetal sheep underwent MI via ligation of the left anterior descending coronary artery.

Use of oral contraceptives and risk of ulcerative colitis - A systematic review and meta-analysis.

Numerous studies have investigated the link between oral contraceptives and risk of ulcerative colitis (UC), but the results have been controversial. We systematically reviewed all relevant published studies and evaluated the association between the use of oral contraceptives and the development of UC by meta-analysis. Databases including PubMed, EMbase, CNKI and WanFang data were thoroughly searched from inception to September 2018 to collect the studies on the correlation between oral contraceptives and the risk of UC.

Use of Cerium Oxide Nanoparticles Conjugated with MicroRNA-146a to Correct the Diabetic Wound Healing Impairment.

Background: Diabetic wounds have become one of the most challenging public health issues of the 21st century, yet there is no effective treatment available. We have previously shown that the diabetic wound healing impairment is associated with increased inflammation and decreased expression of the regulatory microRNA miR-146a. We have conjugated miR-146a to cerium oxide nanoparticles (CNP-miR146a) to target reactive oxygen species (ROS) and inflammation.

Mesenchymal stem cells correct impaired diabetic wound healing by decreasing ECM proteolysis.

Impaired diabetic wound healing is associated with a dermal extracellular matrix protein profile favoring proteolysis; within the healing diabetic wound, this is represented by an increase in activated matrix metalloproteinase (MMPs). Treatment of diabetic wounds with mesenchymal stem cells (MSCs) has been shown to improve wound healing; however, there has not yet been an assessment of their ability to correct dysregulation of MMPs in diabetic wounds. Furthermore, there has been no prior assessment of the role of microRNA29b (miR-29b), an inhibitory regulatory molecule that targets MMP-9 mRNA.

Cardiac Progenitor Cell Recruitment Drives Fetal Cardiac Regeneration by Enhanced Angiogenesis.

Background: In contrast to adults, the fetal response to myocardial infarction (MI) is regenerative, requiring the recruitment of cardiac progenitor cells to replace infarcted myocardium. Macrophage contribution to tissue repair depends on their phenotype: M1 are proinflammatory and initiate angiogenesis; M2a are profibrotic and contribute to blood vessels maturation; and M2c are proremodeling and proangiogenesis. The goal of the present study was to expand on this work by examining cardiac progenitor cells recruitment, and the role of macrophages in promoting angiogenesis and cardiac regeneration in the fetal heart after MI.

Long non-coding RNA Lethe regulates hyperglycemia-induced reactive oxygen species production in macrophages.

Type 2 diabetes mellitus is a complex, systemic metabolic disease characterized by insulin resistance and resulting hyperglycemia, which is associated with impaired wound healing. The clinical complications associated with hyperglycemia are attributed, in part, to the increased production of reactive oxygen species (ROS). Recent studies revealed that long non-coding RNAs (lncRNAs) play important regulatory roles in many biological processes.

Mechanisms of mesenchymal stem cell correction of the impaired biomechanical properties of diabetic skin: The role of miR-29a.

Diabetic skin has impaired wound healing properties following injury. We have further shown that diabetic skin has weakened biomechanical properties at baseline. We hypothesize that the biomechanical properties of diabetic skin decline during the progression of the diabetic phenotype, and that this decline is due to the dysregulation of miR-29a, resulting in decreased collagen content.

SCF increases in utero-labeled stem cells migration and improves wound healing.

Diabetic skin wounds lack the ability to heal properly and constitute a major and significant complication of diabetes. Nontraumatic lower extremity amputations are the number one complication of diabetic skin wounds. The complexity of their pathophysiology requires an intervention at many levels to enhance healing and wound closure.

The role of microRNA-15b in the impaired angiogenesis in diabetic wounds.

The impairment in diabetic wound healing represents a significant clinical problem. Decreased angiogenesis is thought to play a central role in the pathogenesis of this impairment. We have previously shown that treatment of diabetic murine wounds with mesenchymal stem cells can improve healing, but the mechanisms are not completely defined.

Dysregulation of collagen production in diabetes following recurrent skin injury: contribution to the development of a chronic wound.

Recurrent injury has been implicated in the development of chronic diabetic wounds. We have developed a chronic diabetic wound model based upon recurrent injury in diabetic mice. We hypothesized that dysregulation of collagen production at both the mRNA and microRNA levels contributes to the development of chronic diabetic wounds.

Modulation of the inflammatory response by increasing fetal wound size or interleukin-10 overexpression determines wound phenotype and scar formation.

Wound size impacts the threshold between scarless regeneration and reparative healing in the fetus with increased inflammation showed in fetal scar formation. We hypothesized that increased fetal wound size increases pro-inflammatory and fibrotic genes with resultant inflammation and fibroplasia and that transition to scar formation could be reversed by overexpression of interleukin-10 (IL-10). To test this hypothesis, 2-mm and 8-mm dermal wounds were created in mid-gestation fetal sheep.