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For most scientists, publications are the “currency of the realm.” Professional recognition, career advancement, opportunities, and funding decisions are all influenced by numbers of publications, the perceived impact of the journals in which publications appear, and the extent and nature of individual contributions to each publication. In biomedical sciences, the latter have historically been inferred by readers based on assignments to positions in lists of authors. While never ideal, this convention, which differs among disciplines, has become untenable.
Jones and colleagues explain that transition of hair shaft keratinocytes from actively respiring, nucleated cells to structural cells devoid of nucleus and cytoplasm is key to hair production. Although well described in epidermal keratinocytes, this process is poorly understood in the hair follicle. Their study set out to address this knowledge gap, with the aim of gaining insights into cornification mechanisms within the hair follicle and thereby improving the understanding of normal hair physiology.
In an open-label clinical trial, Jabbari and colleagues demonstrated clinical efficacy of the small molecule JAK1,3 inhibitor tofacitinib in 12 patients with moderate-to-severe alopecia areata (AA), a disease that results from autoimmune attack on the hair follicles with resulting significant hair loss. Tofacitinib, which has previously been approved for treatment of rheumatoid arthritis, halted hair loss and allowed considerable regrowth in 11 of these patients without serious adverse effects. Although the therapy is non-curative, as evidenced by relapse after treatment cessation, tofacitinib is a promising therapy for the treatment of hair loss in AA.
During fetal life, mammals undergo a transition from complete skin regeneration to scarring. Previous work demonstrated that embryonic cells that expressed engrailed 1, termed En1-lineage-past fibroblasts (EPFs), contribute to scarring, while En1-lineage-naïve fibroblasts (ENFs) do not. In order to better map dermal morphogenesis, Jiang and colleagues employed single-cell fate mapping, 3D confocal imaging, and in silico analysis. These endeavors revealed that transplantation of ENFs into adult wounds result in regenerative outcomes, while transplantation of EPFs result in scarring.
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) SnapshotDx Quiz. In this monthly online-only quiz, the first question relates to the clinical image found above, while additional questions concern the findings reported in a JID article that provides new information about that disease entity.
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) Cells to Surgery Quiz. In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical image above, while additional questions concern the findings reported in a JID article that provides new information about that disease entity.
Little is known about tanning addiction in adolescents. Miller et al. found that 7.0% of 11th grade students met addiction criteria. After adjusting for all other comorbidities, the odds of addiction were two times greater for students who reported problem use of marijuana or obsessive-compulsive disorder symptoms. The likelihood of addiction increased with problem substance use and psychological symptoms.
Autophagy, discovered as a starvation-induced cellular recycling pathway, routes protein aggregates, damaged organelles, and pathogens to lysosomes and also supports normal tissue homeostasis. Although prior studies linked autophagy to epidermal differentiation, infection, and carcinogenesis, Wang et al. report upstream regulation of autophagy by microRNAs. Subcutaneous delivery of microRNA mimics and antagonists modulated autophagy in vivo, suggesting a novel potential therapeutic strategy in dermatology.
Both atopic dermatitis (AD) and psoriasis are characterized by complex inflammatory circuits that may be regulated through “feed-forward” mechanisms in the epidermis that amplify cellular immune responses through production of keratinocyte-derived cytokines and inflammatory mediators. IL-17C is a unique cytokine that is produced by keratinocytes and that is involved in such synergistic loops that may be responsible for amplifying the inflammation in both diseases. This may ultimately lead to induction of S100As and other molecules that accompany epidermal hyperplasia.
Mann et al. (2018) use recombinant human tyrosinase to screen for novel inhibitors of pigmentation. They develop thiamidol, a new thiazolyl-resorcinol derivative, that is a submicromolar tyrosinase inhibitor and effective for treating solar lentigines. Thiamidol and established inhibitors of pigmentation exhibit substantially different activities on human and mushroom tyrosinase, supporting use of the human enzyme in high-throughput screens.
Web-based surveys, or e-surveys, are surveys designed and delivered using the internet. The use of these survey tools is becoming increasingly common in medical research. Their advantages are appealing to surveyors because they allow for rapid development and administration of surveys, fast data collection and analysis, low cost, and fewer errors due to manual data entry than telephone or mailed questionnaires. Internet surveys may be used in clinical and academic research settings with improved speed and efficacy of data collection compared with paper or verbal survey modalities.
Variants in IRF6 can lead to Van der Woude Syndrome and Popliteal Pterygium syndrome. Furthermore, genes upstream and downstream of IRF6, including GRHL3 and TP63, are also associated with orofacial clefting. Additionally, a variant in an enhancer (MCS9.7) that regulates IRF6 is associated with risk for isolated orofacial clefting. This variant (rs642961) abrogates AP2A protein binding at MCS9.7. Here, we found that AP2A protein regulates MCS9.7 enhancer activity in vivo and IRF6 protein expression in epidermal development.
Overexpression of hexokinase 2 (HK2), and its binding to VDAC1 on the outer mitochondrial membrane of cancer cells, is key to their metabolic reprogramming to aerobic glycolysis, which enables them to proliferate. We describe Comp-1, an allosteric small molecule that selectively detaches HK2 from the mitochondria. Detachment of HK2 reduces glycolysis and triggers apoptosis in cancer cells, without affecting HK1 expressing normal cells. The anti-cancer activity of Comp-1 was demonstrated in the UVB-damaged skin model in SKH-1 mice.
Wound healing is a dynamic process involving gene-expression changes that drive re-epithelialization. Here, we describe an essential role for polyamine regulator, AMD1 in driving cell migration at the wound edge. The polyamines, putrescine, spermidine and spermine are small cationic molecules that play essential roles in many cellular processes. We demonstrate that AMD1, is rapidly upregulated following wounding in human skin biopsies. Knockdown of AMD1 with shRNAs causes a delay in cell migration that is rescued by the addition of spermine.
Skin homeostasis relies on fine tuning of epidermis/dermis interactions and is affected by aging. While extracellular matrix (ECM) proteins, such as integrins, are involved in aging, the molecular basis of the skin changes need to be further investigated. Here, we showed that integrin co-receptor, SLC3A2, required for cell proliferation, is expressed at the surface of resting dermal fibroblasts (DF) in young patients, and drastically reduced with aging. In vivo SLC3A2 DF deletion induced major skin phenotypes resembling premature aging.