MicroRNA-198 an inhibitor of keratinocyte migration
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE37967 | GEO | 2013/03/02
SECONDARY ACCESSION(S): PRJNA165845
REPOSITORIES: GEO
Similar Datasets
Project description:This study identifies miR-198 as a potential inhibitor of keratinocyte migration in skin This study identifies genes differentially expressed during the early phases of wound healing using an ex vivo organ culture model of human skin Total RNA from N/TERT-1 keratinocytes transfected with a negative control miRNA or miR-198 were subjected to microarray analysis Skin from elective plastic surgery were subjected to wounding using ex vivo organ culture model. Total RNA from skin biopsies were isolated at 0hr and 24hr post injury and subjected to mircoarray analysis
2013-03-02 | E-GEOD-37967 | biostudies-arrayexpress
Project description:This study identifies FSTL1 as key component of intiating keratinocyte migration in skin
2013-03-02 | GSE41615 | GEO
Project description:This study identifies FSTL1 as key component of intiating keratinocyte migration in skin Total RNA from N/TERT-1 keratinocytes transfected with a non-targeting siRNA or Smartpool siRNA against FSTL1 were subjected to microarray analysis
2013-03-02 | E-GEOD-41615 | biostudies-arrayexpress
Project description:Olfactomedin-4 (OLFM4) is an olfactomedin-domain-containing glycoprotein which regulates cell adhesion, proliferation, gastrointestinal inflammation, innate immunity and cancer metastasis. In the present study investigated its role in skin regeneration and wound healing. We found that OLFM4 expression is transiently upregulated in the proliferative phase of cutaneous wound healing in humans as well as in mice. Moreover, a significant increase in OLFM4 expression was detected in the skin of lesional psoriasis, a chronic inflammatory disease characterized by keratinocyte hyperproliferation. In vitro experiments demonstrated that OLFM4 can selectively stimulate keratinocyte proliferation and increase both keratinocyte and fibroblast migration ability. Using proteotransciptomic pathway analysis we revealed that transcription factors POU5F1/OCT4 and ESR1 acted as hubs for OLFM4-dependent signalling in keratinocytes. In vivo experiments utilizing mouse splinted full-thickness cutaneous wound healing model showed that application of recombinant OLFM4 protein can significantly improve wound healing time. Taken together, our results suggest that OLFM4 is a transiently upregulated inflammatory signal that promotes wound healing by supporting the functions of both dermal and epidermal cell compartments.
2022-05-20 | PXD029881 | Pride
Project description:G-Protein Coupled Receptor, Class C, Group 5, Member A (GPRC5A) is well-documented in lung and various epithelial cancers. However, its role in the skin remains unexplored. In this study, we investigated the function of this receptor in skin biology and our research demonstrated that its expression responds to mechanical substrate changes in human primary keratinocytes. Furthermore, we observed GPRC5A reinduction during wound healing at the leading edges in an ex vivo burn model, coinciding with the translocation of its C-terminal region into the nucleus. We identified the cleavage site of GPRC5A by N-TAILS analysis, and cathepsin G was characterized as responsible for proteolysis in cultured cells. To gain a deeper understanding of GPRC5A's role in keratinocyte, we performed GPRC5A knockdown in N/TERT-1 cells using short-hairpin RNA. Our findings strongly suggest a close association between GPRC5A and adhesion regulation pathways, but also demonstrate that GPRC5AKD enhanced cell adhesion while reducing cell migration and differentiation. Importantly, these effects were reversed by adding a recombinant polypeptide mimicking the C-terminal region of GPRC5A. Overall, our study reveals an unexpected role of GPRC5A in regulating keratinocyte behavior, implicating its C-terminal region translocation into the nucleus. These results open up interesting strategic pathways for wound healing.
2023-11-27 | GSE248355 | GEO
Project description:Bone morphogenetic protein (BMP) signalling plays a key role in the control of skin development and postnatal remodelling by regulating keratinocyte proliferation, differentiation and apoptosis. To study the role of BMPs in wound-induced epidermal repair, we used transgenic mice overexpressing the BMP downstream component Smad1 under the control of a K14 promoter as an in vivo model, as well as ex vivo and in vitro assays. K14-caSmad1 mice exhibited retarded wound healing associated with significant inhibition of proliferation and increased apoptosis in healing wound epithelium. Furthermore, microarray and qRT-PCR analyses revealed decreased expression of a number of cytoskeletal/cell motility-associated genes including wound-associated keratins (Krt16, Krt17) and Myo5a, in the epidermis of K14- caSmad1 mice versus wild-type controls during wound healing. BMP treatment significantly inhibited keratinocyte migration ex vivo, and primary keratinocytes of K14-caSmad1 mice showed retarded migration compared to wild-type controls. Finally, siRNA-mediated silencing of Bmpr-1B in primary mouse keratinocytes accelerated cell migration and was associated with increased expression of Krt16, Krt17 and Myo5a compared to controls. Thus, this study demonstrates that BMPs inhibit keratinocyte proliferation, cytoskeletal organization and migration in regenerating skin epithelium during wound healing, and raises a possibility for using BMP antagonists for the management of chronic wounds. Two-condition experiment, Wild type vs. Smad1 overexpressing mice. Biological replicates: 2 replicates.
2013-11-01 | E-GEOD-50578 | biostudies-arrayexpress
Project description:The aim of this study was to provide proof of principle as to whether probiotic bacteria or their extracts, could stimulate cutaneous wound healing. To this end, we have used a keratinocyte monolayer scratch assay which assesses one important aspect of wound healing, re-epithelialization. Primary human keratinocyte monolayers were scratched and then exposed to lysates of Lactobacillus rhamnosus GG
2016-03-23 | E-MTAB-3485 | biostudies-arrayexpress
Project description:Although evidence has shown that very small electric currents produce a beneficial therapeutic result for wounds, non-invasive EMF therapy has consisted mostly of anecdotal clinical reports with very few well controlled laboratory mechanistic studies. In this study, we evaluated the effects and potential mechanisms of a non-invasive EMF device on skin wound repair. In vitro analyses with human skin keratinocyte cultures demonstrated that the non-invasive EMF has a very strong effect on accelerating keratinocyte migration and a relatively weaker effect on promoting keratinocyte proliferation. The positive effects of the non-invasive EMF on cell migration and proliferation seem keratinocyte specific without such effects seen on dermal fibroblasts. cDNA microarray and RT-PCR performed revealed increased expression of CRK7 and HOXC8 genes in treated keratinocytes. This study suggests that a non-invasive electric magnetic field accelerates wound reepithelialization through a mechanism of promoting keratinocyte migration and proliferation, possibly due to upregulation of CRK7 and HOXC8 genes. Keywords: Comparative Genomic Hybridization
2008-04-22 | GSE11181 | GEO
Project description:Olfactomedin-4 (OLFM4) is an olfactomedin-domain containing glycoprotein that acts as an important regulator of cell adhesion, proliferation, gastrointestinal inflammation, innate immunity and cancer metastasis. In the present study we aimed to elucidate its role in skin regeneration and wound healing. We found that OLFM4 expression is transiently upregulated in the proliferative phase of cutaneous wound healing in humans as well as in mice. Moreover, a significant increase in OLFM4 expression was detected in the skin of lesional psoriasis, a disease characterized by keratinocyte hyperproliferation. In vitro experiments demonstrated that OLFM4 can selectively stimulate keratinocyte proliferation and increase both keratinocyte and fibroblast migration ability. Using proteotransciptomic pathway analysis we revealed that transcription factors POU5F1/OCT4 and ESR1 acted as hubs for OLFM4-dependent signalling in keratinocytes.
2022-03-02 | GSE188919 | GEO
Project description:Skin is the largest organ in the body and comprises several types of cells. The intercellular plasticity of keratinocytes, fibroblasts, and skin adipocytes contributes to wound healing and dermal adipogenesis. Although keratinocyte activates dermal adipose tissue (dWAT) differentiation upon hair follicular cycle, regulating dWAT hyperplasia through keratinocyte reprogramming is still unknown. We used the CRISPR/Cas9 base editor to induce single nucleotide polymorphisms in Forkhead-box N1 (Foxn1) and identified the p.L19M variant that induced the formation of a thicker dWAT regardless of hair follicular cycle or wound healing. Foxn1 p.L19M activates Wnt5β through transcriptional activity. Wnt5β signaling induces the conversion of dWAT dermal fibroblasts into adipose precursor cells (APCs) and promotes APC adipocyte differentiation through keratinocyte epithelial-mesenchymal transition (EMT) and adipogenic signaling. Wnt5β is involved in the entire process of dWAT hyperplasia through APC supply and adipogenic signaling as a single factor. Foxn1 p.L19M and Wnt5β are expressed in keratinocytes, and a keratinocyte-derived adipogenic signal is critical for dermal adipogenesis. In addition, transient expression of Foxn1 p.L19M or Wnt5β using adeno-associated virus reproduced dermal adipocyte hyperplasia in mice. Considering the increasing importance of dWAT in functions such as the immune response, wound healing, hair follicle growth, and temperature control, this finding has potential applications in skin regeneration
2023-08-05 | GSE239791 | GEO