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Single-cell analysis reveals Cxcl14+ progenitor fibroblast accumulation in regenerating diabetic wound after carbon monoxide-releasing hydrogel therapy

ABSTRACT: Chronic and non-healing skin wound is one of grievous complications of diabetes. In this study, we demonstrated a gas (carbon monoxide)-releasing hyaluronic acid hydrogel (i.e. COHAG) in promoting diabetic wound healing. Our results show that the COHAG significantly accelerated the healing process in diabtic rat full-thickness skin defect model, as compared with hydrogel without gas-releasing molecule and untreated group. Single-cell analysis of regenerating skin samples revealed that Cxcl14-overexpressing (Cxcl14+) fibroblast with progenitor properties are abundantly accumulated at the wound site after COHAG therapy.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE228235 | GEO | 2023/12/05

REPOSITORIES: GEO

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Wound healing and anti-oxidant activities induced by Dersani Hydrogel with Alginate and Dersani Hydrogel ointments

Project description:Explore the role of these hydrogels in wound healing, this study assessed the effects of both, Dersani Hydrogel with Alginate (DHA) and Dersani Hydrogel (DH), in human skin keratinocytes and fibroblasts gene expression profiles in a wound healing context. Sodium alginate (SA) and culture medium were also included as controls.

2021-07-02 | GSE179187 | GEO

THP-1 cells treated with CXCL14

Project description:Monocytic leukemia cell line, THP-1 cells are known to respond to CXCL14. To identfy transcriptional regulation of CXCL14 signalling, we analyse gene expression changed with CXCL14 treatment. THP-1 treated with CXCL14 or PBS treated sample were used.

2013-12-17 | E-GEOD-44550 | biostudies-arrayexpress

Rationally designed, self-assembly, multifunctional hydrogel depot repairs severe spinal cord injury

Project description:Following severe spinal cord injury (SCI), dysregulated neuroinflammation causes neuronal and glial apoptosis, resulting in scar and cystic cavity formation during wound healing process and ultimately atrophic nerve regrowth inhibitory microenvironment. Because of this complex and dynamic nature of SCI pathophysiology, a systemic solution for scar and cavity free wound healing while remodeling microenvironment for nerve regrowth has been rarely explored. To address this challenge, we provided a one-step solution through a self-assembly, multifunctional hydrogel depot punctually releasing the anti-inflammatory drug methylprednisolone sodium succinate (MPSS) and growth factors locally according to its pathophysiology to repair severe SCI. We found release of growth factors alone could only provide some tissues/axons protection, but failed to eliminate all cystic cavity formation. Sustained release of MPSS is sufficient to modulate dysregulated neuroinflammation and eliminate almost all cystic cavity but unable to alleviate impenetrable scar boundaries, which are largely responsive for nerve regrowth failure. Strikingly, synergically releasing anti-inflammatory drugs MPSS and growth factors in the hydrogel depot along SCI pathophysiology protected spared tissues/axons from secondary injury, promoted scar boundary and cavity free wound healing and made permissive bridges for remarkable axonal regrowth. Behavior and electrophysiology studies indicated that the remnant of spared axons but not regenerating axons mediated functional recovery, strongly suggesting that additional interventions are still required to make the rebuilt neuronal circuits perform functions. Taken together, these findings pave the way to develop a systemic solution to treat acute SCI.

2022-01-01 | GSE165635 | GEO

THP-1 cells treated with CXCL14

2013-12-17 | GSE44550 | GEO

Expression change in materal and fetal part of Cxcl14-/- placenta

Project description:Cxcl14+/- mice were mated with Cxcl14+/- mice, the embryos of pregnant females were collected on E13.5. After genotyping, the maternal part and fetal part of Cxcl14-/- and Cxcl14+/+ placentas were dissect out to extract total RNA respectively (n = 3). Total RNA was extracted using PureYield™ RNA Midiprep System (Promega).The maternal part of placenta that contained mesometrial lymphoid aggregate of pregnancy (MLAp) and decidua basalis (DB); the fetal part ofplacenta consisted of spongiotrophoblast and labyrinthin layer.Microarray hybridization was performed using a Mouse NimbleGen cDNA Microarray Kit (Roche), at CapitalBio Co., Ltd.(Beijing,China). Primary data were scaned using NimbleGen MS200 (Roche), and then extracted using NimbleScan system (Roche). Cxcl14+/- mice were mated with Cxcl14+/- mice, the embryos of pregnant females were collected on E13.5. After genotyping, the maternal part and fetal part of Cxcl14-/- and Cxcl14+/+ placentas were dissect out to extract total RNA respectively (n = 3). Total RNA was extracted using PureYield™ RNA Midiprep System (Promega).The maternal part of placenta that contained mesometrial lymphoid aggregate of pregnancy (MLAp) and decidua basalis (DB); the fetal part ofplacenta consisted of spongiotrophoblast and labyrinthin layer.Microarray hybridization was performed using a Mouse NimbleGen cDNA Microarray Kit (Roche), at CapitalBio Co., Ltd.(Beijing,China). Primary data were scaned using NimbleGen MS200 (Roche), and then extracted using NimbleScan system (Roche).

2013-06-19 | E-GEOD-48095 | biostudies-arrayexpress

Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling (RNA-Seq)

Project description:Skin wound healing is one of the major prevalent medical problems in the worldwide. Wound healing involves multi-process synergy and re-epithelialization is an essential part of wound healing. Histone H3K36 tri-methylase Setd2 has been extensively studied in different biological processes and diseases. However, the function of Setd2 in the wound healing remains unclear. To elucidate the biological role of Setd2 in the skin wound healing, conditional gene targeting was employed to establish epidermis-specific Setd2-deficient mice. We found that Setd2 deficiency resulted in accelerated re-epithelialization during cutaneous wound healing by promoting keratinocytes proliferation and migration. Furthermore, we demonstrated that loss of Setd2 activated the AKT/mTOR pathway, and pharmacological inhibitions of AKT and mTOR with MK2206 and rapamycin delayed wound closure, respectively. In conclusion, our results reveal the essential role of Setd2 in skin wound healing that is Setd2 loss promotes cutaneous wound healing via activation of AKT/mTOR signaling.

2020-12-25 | GSE163860 | GEO

Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling (ChIP-Seq)

2020-12-25 | GSE163858 | GEO

RNAseq changes in mouse wound with or without time course treatment by Vemurafenib

Project description:BRAF inhibitors are highly effective therapies for patients with BRAF V600 mutated metastatic melanoma. Patients who receive BRAF inhibitors develop a variety of hyper-proliferative skin conditions, whose pathogenic basis is the paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway in BRAF wild-type cells. Most of these hyper-proliferative skin changes improve when a MEK inhibitor is co-administered, as a MEK inhibitor blocks paradoxical MAPK activation. We tested whether we could take advantage of the mechanistic understanding of the skin hyper-proliferative side effects of BRAF inhibitors to accelerate skin wound healing by inducing paradoxical MAPK activation. Here we show that the BRAF inhibitor vemurafenib accelerates human keratinocyte proliferation and migration by increasing ERK phosphorylation and cell cycle progression. Topical treatment with vemurafenib in two wound-healing models in mice accelerated cutaneous wound healing and improved the tensile strength of healing wounds through paradoxical MAPK activation; addition of a MEK inhibitor reversed the benefit of vemurafenib-accelerated wound healing. The same dosing regimen of topical BRAF inhibitor did not increase the incidence of cutaneous squamous cell carcinomas in mice even after the application of a carcinogen. Therefore, topical BRAF inhibitors may have clinical applications in accelerating the healing of skin wounds. Full depth incisional wound mice tissues with/without Vemurafenib treatment were sent for RNAseq analysis on day 2, 6 and 14

2016-07-29 | E-GEOD-74558 | biostudies-arrayexpress

Expression data from wound skin taken at three time points post wounding

Project description:The full complement of hair follicles is generated during embryogenesis. Normally, no new hair is created after this time. Large full thickness skin excision wounding can result in the generation of new hair in the adult. Placodes can be observed following complete reepithelialization at wound day 14. The events leading to hair neogenesis following wounding remain poorly understood. Late healing events (from wound day 10 to wound day 14) provide a possible window of induction for hair regeneration. We used microarrays to analyse changes in gene expression during late skin healing to provide candidates for factors involved in hair neogenesis following wounding. 6 week old C57Bl/6 mice received large full thickness skin excisions. Healing wound tissue was excised at wound day 10, 12 or 14 and analyzed for gene expression.

2013-09-01 | E-GEOD-46244 | biostudies-arrayexpress

Expression change in materal and fetal part of Cxcl14-/- placenta

2013-06-19 | GSE48095 | GEO

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