https://cyberleninka.org/article/n/238598.pdf

Use of electrospinning technique for biomedical applications

Bone continuously undergoes building and degradation — a process known as bone remodelling This tightly controlled process can be dysregulated by chronic inflammation, and bone loss is commonly associated with inflammatory diseases Here, Redlich and Smolen discuss the molecular mechanisms mediating the inflammatory loss of bone and present strategies and agents for therapeutic intervention Bone is a tissue undergoing continuous building and degradation This remodelling is a tightly regulated process that can be disturbed by many factors, particularly hormonal changes Chronic inflammation can also perturb bone metabolism and promote increased bone loss Inflammatory diseases can arise all over the body, including in the musculoskeletal system (for example, rheumatoid arthritis), the intestine (for example, inflammatory bowel disease), the oral cavity (for example, periodontitis) and the lung (for example, cystic fibrosis) Wherever inflammatory diseases occur, systemic effects on bone will ensue, as well as increased fracture risk Here, we discuss the cellular and signalling pathways underlying, and strategies for therapeutically interfering with, the inflammatory loss of bone

Inflammatory bone loss: pathogenesis and therapeutic intervention.

Polymer nanofibrous structures: Fabrication, biofunctionalization, and cell interactions

https://www.hairsite.com/hair-loss/img/uploaded_files/2879_file56.pdf

Review of hair follicle dermal cells

Androgenetic alopecia, commonly known as male pattern baldness, is the most common type of progressive hair loss disorder in men. The aim of this paper is to review recent advances in understanding the pathophysiology and molecular mechanism of androgenetic alopecia. Using the PubMed database, we conducted a systematic review of the literature, selecting studies published from 1916 to 2016. The occurrence and development of androgenetic alopecia depends on the interaction of endocrine factors and genetic predisposition. Androgenetic alopecia is characterized by progressive hair follicular miniaturization, caused by the actions of androgens on the epithelial cells of genetically susceptible hair follicles in androgen-dependent areas. Although the exact pathogenesis of androgenetic alopecia remains to be clarified, research has shown that it is a polygenetic condition. Numerous studies have unequivocally identified two major genetic risk loci for androgenetic alopecia, on the X-chromosome AR⁄EDA2R locus and the chromosome 20p11 locus. Candidate gene and genome-wide association studies have reported that single-nucleotide polymorphisms at different genomic loci are associated with androgenetic alopecia development. A number of genes determine the predisposition for androgenetic alopecia in a polygenic fashion. However, further studies are needed before the specific genetic factors of this polygenic condition can be fully explained.

/pdf/androgenetic-alopecia-a-review-3mgwd4zoaw.pdf

Androgenetic alopecia: a review.

Dihydrotestosterone-inducible dickkopf 1 from balding dermal papilla cells causes apoptosis in follicular keratinocytes.

We tested the effects on the early-stage wound healing of poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) nanofiber matrices cultured with hair follicular cells. PHBV only, PHBV/collagen, and PHBV/gelatin at a 7/3 weight ratio were produced by electrospinning, and their in vitro cell culture and in vivo wound healing as biological dressings were examined. In cell attachment and growth on matrices, dermal sheath (DS) cells attached to hydrophilic PHBV/collagen and PHBV/gelatin faster than hydrophobic PHBV at the early incubation stage (up to 6 h). From 6- to 24-h incubation, PHBV/collagen showed the best results in cell culture. Furthermore, PHBV/collagen cocultured for 3-5 days with DS and epithelial outer root sheath (ORS) cells expressed more extracellular materials, such as type I collagen, elastin, and alpha-smooth muscle actin, than cocultured PHBV with the same cells. However, there was no significant difference between PHBV and PHBV/collagen in the amounts of cytokeratin 8 expressed. Grafting of PHBV and PHBV/collagen matrices cocultured with ORS/DS cells for 3-5 days showed that PHBV promoted wound closure and re-epithelization more obviously than PHBV/collagen in both cocultured matrices and matrices alone. Cocultured matrices would heal wounds better than the corresponding matrices alone. Thus, PHBV cocultured with ORS/DS cells could be used as a cell-seeded biological dressing, thereby reducing preparation time as well as regenerating the epidermis efficiently during the early stage of wound healing.

Effect of poly(3-hydroxybutyrate-co-3-hydroxyvalerate) nanofiber matrices cocultured with hair follicular epithelial and dermal cells for biological wound dressing.

Purpose: Recent studies have shown that Dickkopf-1 (DKK-1) is overexpressed in some tumors, including hepatocellular carcinoma. However, the role of increased DKK-1 in these tumors is not known. In this study, the DKK-1 expression in hepatocellular carcinoma (HCC) cell lines was evaluated and the effect of DKK-1 overexpression in HCC cell lines was studied. Materials and Methods: The expression of DKK-1 in hepatocellular carcinoma cell lines was evaluated by RT-PCR. Stable cell lines that overexpressed DKK-1 were established. Cell growth, adhesion, migration and invasion assays were performed. Results: RT-PCR analysis showed that 5 out of 8 HCC cell lines expressed DKK-1. The forced expression of DKK-1 suppressed the growth of cells and increased the population of cells in the sub-G1 phase. In addition, DKK- 1 reduced the cellular adhesion capacity to collagen type I and fibronectin, and it increased migratory capacity. However, overexpression of DKK-1 did not increase the invasion capacity of the HCC cell line. Conclusion: Collectively, our data suggest that overexpression of DKK-1 affects the biology of HCC cells. (Cancer Res Treat. 2007;39:30-36)

/pdf/analysis-of-cellular-changes-resulting-from-forced-1h25bkg019.pdf

Analysis of Cellular Changes Resulting from Forced Expression of Dickkopf-1 in Hepatocellular Carcinoma Cells.

Establishment of SV40T-transformed human dermal papilla cells and identification of dihydrotestosterone-regulated genes by cDNA microarray.

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Dihydrotestosterone-inducible dickkopf 1 from balding dermal papilla cells causes apoptosis in follicular keratinocytes.

Effect of poly(3-hydroxybutyrate-co-3-hydroxyvalerate) nanofiber matrices cocultured with hair follicular epithelial and dermal cells for biological wound dressing.

Analysis of Cellular Changes Resulting from Forced Expression of Dickkopf-1 in Hepatocellular Carcinoma Cells.

Establishment of SV40T-transformed human dermal papilla cells and identification of dihydrotestosterone-regulated genes by cDNA microarray.