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The secretion of TGF-β3 by adipose-derived stem cells inhibits melanin synthesis and its impact on the cAMP/PKA signaling pathway.
Arch Dermatol Res
January 2025
Burn and Wound Repair Center, The Third Hospital of Hebei Medical University, No. 139, Ziqiang Road, Shijiazhuang, Hebei Province, 050035, China.
This study aimed to investigate the role of transforming growth factor-beta 3 (TGF-β3) secreted by adipose-derived stem cells (ADSCs) in suppressing melanin synthesis during the wound healing process, particularly in burn injuries, and to explore the underlying mechanisms involving the cAMP/PKA signaling pathway. ADSCs were isolated from C57BL/6 mice and characterized using flow cytometry and differentiation assays. A burn injury model was established in mice, followed by UVB irradiation to induce hyperpigmentation.
View Article and Find Full Text PDFIntegrative genetics and multiomics analysis reveal mechanisms and therapeutic targets in vitiligo highlighting JAK STAT pathway regulation of CTSS.
Sci Rep
January 2025
Department of Dermatology, First Affiliated Hospital of Zhengzhou University, No.1 Longhu Outer Ring Road, Jinshui District, Zhengzhou, 450052, Henan, China.
Vitiligo is a complex autoimmune disease characterized by the loss of melanocytes, leading to skin depigmentation. Despite advances in understanding its genetic and molecular basis, the precise mechanisms driving vitiligo remain elusive. Integrating multiple layers of omics data can provide a comprehensive view of disease pathogenesis and identify potential therapeutic targets.
View Article and Find Full Text PDFregulates melanocortin 4 receptor transcription and energy homeostasis.
Sci Transl Med
January 2025
Hypothalamic Research Center, Department of Internal Medicine, UT Southwestern Medical Center, Dallas TX, 75390, USA.
Disruption of hypothalamic melanocortin 4 receptors (MC4Rs) causes obesity in mice and humans. Here, we investigated the transcriptional regulation of in the hypothalamus. In mice, we show that the homeodomain transcription factor Orthopedia (OTP) is enriched in MC4R neurons in the paraventricular nucleus (PVN) of the hypothalamus and directly regulates transcription.
View Article and Find Full Text PDFPeripubertal antagonism of corticotropin-releasing factor receptor 1 results in sustained changes in behavioral plasticity and the transcriptomic profile of the amygdala.
Neuroscience
January 2025
School of Arts & Sciences, Health Psychology Program, Massachusetts College of Pharmacy and Health Sciences, Boston Massachusetts, 02115, United States. Electronic address:
Article Synopsis
- Peripuberty is a crucial time for brain development, and blocking CRFR1 receptors in young rats helps minimize negative effects of early-life stress on neural function and behavior.
- In an experiment, male rats showed immediate behavioral changes like reduced prepulse inhibition (PPI) after receiving a CRFR1 antagonist, while females only exhibited differences in behavior after becoming adults.
- Long-term gene expression changes in the amygdala indicate that the effects of CRFR1 blockage during peripuberty impact different neural pathways in males and females, emphasizing the importance of understanding these effects for adolescent mental health.
The effects of corticotropin-releasing factor (CRF) and urocortins on the serotonin (hydroxytryptamine, 5HT) released from the raphe nuclei (RN).
Neuropeptides
January 2025
Department of Pathophysiology, Faculty of Medicine, University of Szeged, Hungary.
Corticotropin-releasing factor (CRF) and urocortins (UCN1, UCN2 and UCN3) belong to the same CRF family of neuropeptides. They regulate the neuroendocrine, autonomic and behavioral responses to stress via two CRF receptors (CRF1 and CRF2). Stress, anxiety and depression affects the activity of the hypothalamic-pituitary-adrenal (HPA) axis and the serotoninergic neurotransmission, both being regulated by CRF and CRF-related peptides.
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