SncRNA changes induced by tension in hypertrophic scar.
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ABSTRACT:
SUBMITTER: Yin C
PROVIDER: S-EPMC9827810 | biostudies-literature | 2022 Aug
REPOSITORIES: biostudies-literature
Publications
sncRNA changes induced by tension in hypertrophic scar.
Yin Chuang C Zhang Shixi S Ya Chen C Wang Chuandong C Liang Yimin Y Wang Chen C
Acta biochimica et biophysica Sinica 20220801 8
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Project description:Pentoxifylline attenuated hypertrophic scars by influencing the cell cycles
2019-07-09 | GSE122891 | GEO
Project description:Background: As a fibrotic disease with a high incidence, the pathogenesis of hypertrophic scarring is still not fully understood, and the treatment of this disease is also challenging. In recent years, human adipose-derived mesenchymal stem cells (AD-MSCs) have been considered an effective treatment for hypertrophic scars. This study mainly explored whether the therapeutic effect of AD-MSCs on hypertrophic scars is associated with oxidative-stress-related proteins. Methods: AD-MSCs were isolated from adipose tissues and characterized through flow cytometry and a differentiation test. Afterwards, coculture, cell proliferation, apoptosis, and migration were detected. Western blotting and a quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect oxidative stress-related genes and protein expression in hypertrophic scar fibroblasts (HSFs). Flow cytometry was used to detect reactive oxygen species (ROS). A nude mouse animal model was established; the effect of AD-MSCs on hypertrophic scars was observed; and hematoxylin and eosin staining, Masson's staining, and immunofluorescence staining were performed. Furthermore, the content of oxidative-stress-related proteins, including nuclear factor erythroid-2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), B-cell lymphoma 2(Bcl2), Bcl2-associated X(BAX) and caspase 3, was detected. Results: Our results showed that AD-MSCs inhibited HSFs' proliferation and migration and promoted apoptosis. Moreover, after coculture, the expression of antioxidant enzymes, including HO-1, in HSFs decreased; the content of reactive oxygen species increased; and the expression of Nrf2 decreased significantly. In animal experiments, we found that, at 14 days after injection of AD-MSCs into human hypertrophic scar tissue blocks that were transplanted onto the dorsum of nude mice, the weight of the tissue blocks decreased significantly. Hematoxylin and eosin staining and Masson's staining demonstrated a rearrangement of collagen fibers. We also found that Nrf2 and antioxidant enzymes decreased significantly, while apoptotic cells increased after AD-MSC treatment. Conclusions: Our results demonstrated that AD-MSCs efficiently cured hypertrophic scars by promoting the apoptosis of HSFs and by inhibiting their proliferation and migration, which may be related to the inhibition of Nrf2 expression in HSFs, suggesting that AD-MSCs may provide an alternative therapeutic approach for the treatment of hypertrophic scars.
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Project description:Hypertrophic scars (HTSs) occur in 30 to 72% patients after thermal injury. Risk factors include skin color, female sex, young age, burn site, and burn severity. Recent correlations between genetic variations and clinical conditions suggest that single-nucleotide polymorphisms (SNPs) may be associated with HTS formation. The authors hypothesized that an SNP in the p27 gene (rs36228499) previously associated with decreased restenosis after coronary stenting would be associated with lower Vancouver Scar Scale (VSS) measurements and decreased itching. Patient and injury characteristics were collected from adults with thermal burns. VSS scores were calculated at 4 to 9 months after injury. Genotyping was performed using real-time polymerase chain reaction. Logistic regression was used to determine risk factors for HTS as measured by a VSS score >7. Three hundred subjects had a median age of 39 years (range, 18-91); 69% were male and median burn size was 7% TBSA (range, 0.25-80). Consistent with literature, the p27 variant SNP had an allele frequency of 40%, but was not associated with reduced HTS formation or lower itch scores in any genetic model. HTS formation was associated with American Indian/Alaskan Native race (odds ratio [OR], 12.2; P = .02), facial burns (OR, 9.4; P = .04), and burn size ≥20% TBSA (OR, 1.99; P = .03). Although the p27 SNP may protect against vascular fibroproliferation, the effect cannot be generalized to cutaneous scars. This study suggests that American Indian/Alaskan Native race, facial burns, and higher %TBSA are independent risk factors for HTS. The American Indian/Alaskan Native association suggests that there are potentially yet-to-be-identified genetic variants.
| S-EPMC3786175 | biostudies-literature
Project description:The goal was to obtain expression data from the deep cones in early human hypertrophic scars to be used to confirm expression data obtained in a porcine model. Three samples of early human hypertrophic scar were obtained and processed with the Affymetrix Human GeneChip® Human Genome U133 plus 2.0. Sample demographics were Black 2, White 1; upper extremity 2, neck 1; times since injury 6.7 months and 10.8 months; and patient ages were 19 and 54.
2011-12-31 | E-GEOD-26213 | biostudies-arrayexpress
Project description:BackgroundHypertrophic cardiomyopathy (HCM), a genetically transmitted disease, is the most common genetic cardiovascular disease. Current strategies to stratify risk are expensive and concentrated in wealthy centers. Twelve-lead electrocardiography (ECG) is inexpensive, universally available, and can be readily used for Selvester QRS scoring, which estimates scar size. This study aimed to establish the relation between ECG scar quantification and myocardial fibrosis (extent of myocardial delayed enhancement) in multidetector computed tomography (MDCT).HypothesisThere is a significant association between ECG scar quantification and the extent of myocardial delayed enhancement in MDCT.MethodsSeventy-five patients with HCM underwent a routine clinical evaluation and echocardiography, 12-lead ECG, and MDCT study. Patients with and without an implantable cardioverter-defibrillator were included.ResultsThe estimated Selvester QRS score of myocardial fibrosis was correlated significantly (R = 0.70; P < 0.01) with the quantified MDCT fibrosis. Compared with MDCT, the QRS score had 84.8% sensitivity and 88.8% specificity. Myocardial fibrosis was present in 88% of these patients with HCM (fibrotic mass, 9.87 ±10.8 g) comprising 5.66% ±6.16% of the total myocardial mass seen on the MDCT images. The Selvester QRS score reliably predicted the fibrotic mass in 76% of patients, which estimated 8.44% ±7.39% of the total myocardial mass.ConclusionsThe Selvester QRS score provides reliable quantification of myocardial fibrosis and was well correlated with MDCT in patients with HCM.
| S-EPMC6489858 | biostudies-literature
Project description:BackgroundHypertrophic scars (HS) affect millions of people each year and require better treatment strategies. Bacterial extracellular vesicles (EVs) are advantaged by low cost and high yield which was commonly used in the treatment of diseases. Here, we investigated the therapeutic efficacy of EVs obtained from Lactobacillus druckerii in hypertrophic scar. In vitro, the effects of Lactobacillus druckerii-derived EVs (LDEVs) on Collagen I/III and α-SMA in fibroblasts obtained from HS. In vivo, a scleroderma mouse model was used to investigate the effects of LDEVs on fibrosis. The impact of LDEVs on excisional wound healing was explored. The different proteins between PBS and LDEVs treated fibroblasts derived from hypertrophic scar were studied by untargeted proteomic analysis.ResultsIn vitro, LDEVs treatment significantly inhibited the expression of Collagen I/III and α-SMA and cell proliferation of fibroblasts derived from HS. In vivo, LDEVs withdrawn the hypertrophic scar formation in scleroderma mouse model and decreased the expression of α-SMA. LDEVs promoted the proliferation of skin cells, new blood vessel formation and wound healing in excisional wound healing mice model. Moreover, proteomics has shown that LDEVs inhibit hypertrophic scar fibrosis through multiple pathways.ConclusionsOur results indicated that Lactobacillus druckerii-derived EVs has the potential application in the treatment of hypertrophic scars and any other fibrosis diseases.
| S-EPMC10053340 | biostudies-literature
Project description:Pentoxifylline-induced differentially-expressed genes in hypertrophic scar fibroblasts
| PRJNA506825 | ENA
Project description:Background: Hypertrophic scar (HS) is a fibrotic cutaneous disease with few effective therapies. Lycorine is a drug with pro-apoptotic ability and anti-fibrosis potential. This study aimed to test whether lycorine could trigger the apoptosis of hypertrophic scar fibroblasts (HSFs) to inhibit HS formation. Methods: The proapoptotic and anti-fibrosis effects of lycorine on the viability and apoptosis of human primary HSFs and their reactive oxygen species (ROS) production as well as a rabbit ear model of HS were determined by CCK-8, flow cytometry, Western blot, immunofluorescence, transwell migration, collagen gel contraction assays. Results: Lycorine treatment selectively decreased the viability of HSFs, and induced their apoptosis, but not normal fibroblasts (NFs). Lycorine treatment increased the relative levels of Bax and cleaved PARP expression, cytochrome C cytoplasm translocation, but decreased Bcl-2, caspase-3 and caspase-9 expression, the mitochondrial membrane potential (MMP) in HSFs. Lycorine inhibited the migration and contraction of HSFs, and reduced the expression of collagen I, collagen III and α-SMA. Mechanistically, lycorine treatment stimulated high levels of ROS production, leading to apoptosis of HSFs while treatment with NAC, a ROS inhibitor, significantly mitigated or abrogated the pro-apoptotic and antifibrotic activity of lycorine in HSFs. Moreover, lycorine treatment mitigated the severity of HS in rabbit ears by inducing fibroblast apoptosis. Conclusion: These results indicate that lycorine has a potent anti-fibrotic activity and is a potential drug for intervention of HS.
| S-EPMC9171077 | biostudies-literature
Project description:Hypertrophic scar (HS) is a plaque fibrous and indurated dermal lesion that may cause physical, psychological, and cosmetic challenges for patients. Intralesional injection of triamcinolone acetonide (TA) is commonly used in clinical practice, which cause unbearable pain and uneven drug delivery within HS tissue. Herein, we developed a paper battery powered iontophoresis-driven microneedles patch (PBIMNP) for self-management of HS. The high integration of PBIMNP was achieved by incorporating a paper battery as the power source for iontophoresis. The transdermal drug delivery strategy of PBIMNP combined microneedles and iontophoresis techniques, involving "pressing and poking, phase transformation, and diffusion and iontophoresis", which can actively deliver 90.19% drug into the HS tissue with excellent in vitro drug permeation performance. PBIMNP administration effectively reduced the mRNA and protein levels, leading to a decrease in the expression of TGF-β1 and Col I associated with HS formation, demonstrating its efficacy in HS treatment. The microneedles and wearable design endow the PBIMNP as a highly promising platform for self-administration on HS treatment.
| S-EPMC11894194 | biostudies-literature
Project description:BackgroundHypertrophic scar (HS) is characterized by the increased proliferation and decreased apoptosis of myofibroblasts. Myofibroblasts, the main effector cells for dermal fibrosis, develop from normal fibroblasts. Thus, the stimulation of myofibroblast apoptosis is a possible treatment for HS. We aimed to explore that whether over-activated myofibroblasts can be targeted for apoptosis by anticancer drug elesclomol.Methods4',6-diamidino-2-phenylindole staining, flow cytometry, western blotting, collagen gel contraction and immunofluorescence assays were applied to demonstrate the proapoptotic effect of elesclomol in scar derived myofibroblasts and TGF-β1 induced myofibroblasts. The therapeutic potential of elesclomol was investigated by establishing rabbit ear hypertrophic scar models.FindingsBoth 4',6-diamidino-2-phenylindole staining and flow cytometry indicated that elesclomol targets myofibroblasts in vitro. Collagen gel contraction assay showed that elesclomol inhibited myofibroblast contractility. Flow cytometry and western blot analysis revealed that elesclomol resulted in excessive intracellular levels of reactive oxygen species(ROS), and caspase-3 and cytochrome c proteins. Moreover, compared with the control group, the elesclomol group had a significantly lower scar elevation index in vivo. Immunofluorescence assays for TUNEL and α-smooth muscle actin indicated that elesclomol treatment increased the number of apoptotic myofibroblasts.InterpretationThe above results indicate that elesclomol exerted a significant inhibitory effect on HS formation via targeted myofibroblast apoptosis associated with increased oxidative stress. Thus, elesclomol is a promising candidate drug for the treatment of myofibroblast-related diseases such as HS.
| S-EPMC7132150 | biostudies-literature