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Nicole L. Rosin

Researcher at University of Calgary

Publications -  34
Citations -  1235

Nicole L. Rosin is an academic researcher from University of Calgary. The author has contributed to research in topics: Wound healing & Medicine. The author has an hindex of 15, co-authored 24 publications receiving 810 citations. Previous affiliations of Nicole L. Rosin include University of British Columbia & Dalhousie University.

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Dysfunction of Hair Follicle Mesenchymal Progenitors Contributes to Age-Associated Hair Loss.

TL;DR: It is shown that HF dermal stem cells (hfDSCs) reconstitute the damaged DP and maintain hair growth, suggesting that hfDSC dysfunction may trigger degeneration of the inductive niche and suggest that progressive dysfunction within the mesenchymal progenitor pool contributes to age-related hair loss.
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Disruption of Collagen Homeostasis Can Reverse Established Age-Related Myocardial Fibrosis

TL;DR: A novel observation is that BAPN treatment modulated the transforming growth factor-β pathway, collagen synthesis, and the resident macrophage population, which is especially valuable in terms of potential therapeutic targeting of collagen regulation and thereby age-related myocardial fibrosis.
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Macrophages Promote Wound-Induced Hair Follicle Regeneration in a CX3CR1- and TGF-β1-Dependent Manner.

TL;DR: A model in which transforming growth factor-β1 and CX3CR1 are critical for recruiting and maintaining the CCR2+CX3 CR1hiLy6CloTNFα+ macrophages critical for stimulating WIHG is proposed.
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Hair follicle dermal stem cells and skin-derived precursor cells: Exciting tools for endogenous and exogenous therapies.

TL;DR: It is contended that dermal stem cells provide an important reservoir of renewable dermal progenitors that may enable development of novel restorative therapies following hair loss, skin injury or disease.
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Myocardial migration by fibroblast progenitor cells is blood pressure dependent in a model of angII myocardial fibrosis

TL;DR: Evidence is provided that myocardial infiltration by fibroblast progenitor cells secondary to AngII and the resultant fibrosis can be prevented by the addition of hydralazine, suggesting that the mechanism of fibrosis is blood pressure dependent.