A study of s - wave π π scattering in the reaction π+n → π0π0p at 2.15 GeV/c

Bensinger, J. R.; Erwin, A. R.; Thompson, M.; Walker, W. D.

doi:10.1016/0370-2693(71)90128-6

Cited by 27 publications

(1 citation statement)

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“…T-cell activation is accompanied by the downregulation of LXR-a target genes involved in cholesterol transport. LXR-a-dependent coupling of cholesterol metabolism and proliferation represents a previously unrecognized mechanism for the regulation of immune responses (20). Cholesterol is important for membrane stability and is the key substrate for the synthesis of steroid hormones and vitamin D. Furthermore, it is a major component of the lipid barrier in the stratum corneum of the human epidermis.…”

Section: Introductionmentioning

confidence: 99%

Altered levels of LXR‐α: crucial implications in the pathogenesis of vitiligo

Kumar

Parsad

Kanwar

et al. 2012

Experimental Dermatology

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In recent times, the role of LXRs in skin physiology and pathology has evolved rapidly because of their role in proliferation, carcinogenesis, differentiation and permeability barrier function. LXRs were identified as promising drug targets for the treatment of many skin diseases. For this study, skin biopsies were taken from 15 patients with vitiligo and six controls to culture melanocytes from clinically active perilesional and normal skin. Gene expression was examined by reverse transcriptase-polymerase chain reaction analysis. Role of LXR-α in regulating the expression of MMPs was checked by gene knock-down, and its role in vitiligo pathogenesis was checked by treatment with LXR-α agonist 22(R)-hydroxycholesterol. After treatment adhesion assay, annexin V staining and proliferation assay were performed. The expression of LXR-α was relatively more in perilesional skin melanocytes as compared to uninvolved skin melanocytes of non-segmental vitiligo patient, and controls on the other hand, perilesional melanocytes were more prone to apoptosis. LXR-α gene knock-down significantly increases the expression of MMPs. LXR-α agonist 22(R)-hydroxycholesterol treatment significantly decreases melanocyte adhesion, apoptosis and proliferation. Higher expression of LXR-α in perilesional skin melanocytes significantly decreases the adhesion, proliferation and matrix metalloproteinases and increases apoptosis.

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Section: Introductionmentioning

confidence: 99%