Melanocortin-5 receptor and sebogenesis

Zhang, Li; Li, Wen‐Hwa; Anthonavage, Michael; Pappas, Apostolos; Rossetti, Dianne; Cavender, Druie; Seiberg, Miri; Eisinger, Magdalena

doi:10.1016/j.ejphar.2010.10.100

Cited by 43 publications

(28 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[51] Retinoids also downregulate melanocortin receptor expression, which causes sebocyte differentiation and lipogenesis. [52] Metformin treatment has 'counter-regulatory' action to the puberty-induced shift of the insulin ⁄ IGF-1 axis to higher levels. Patients with PCOS on metformin treatment showed a decrease in elevated serum IGF-1 and androgen levels.…”

Section: Insulin and Igf-1 Signaling In Acne Treatmentmentioning

confidence: 99%

Role of insulin resistance and diet in acne

Kumari¹,

Thappa²

2013

Indian J Dermatol Venereol Leprol

View full text Add to dashboard Cite

There is increasing evidence in support of the interplay of growth hormone (GH), insulin, and insulin-like growth factor-1 (IGF-1) signaling during puberty, which have a causal role in pathogenesis of acne by influencing adrenal and gonadal androgen metabolism. Milk consumption and hyperglycemic diets can induce insulin and IGF-1-mediated PI3K ⁄ Akt-activation inducing sebaceous lipogenesis, sebocyte, and keratinocyte proliferation, which can aggravate acne. Occurence of acne as part of various syndromes also provides evidence in favor of correlation between IGF-1 and acne.

show abstract

Section: Insulin and Igf-1 Signaling In Acne Treatmentmentioning

confidence: 99%

Role of insulin resistance and diet in acne

Kumari¹,

Thappa²

2013

Indian J Dermatol Venereol Leprol

View full text Add to dashboard Cite

show abstract

“…For example in mice, MC5R has the broadest tissue expression distribution of all the MCRs (Chen et al 1997), yet the corresponding physiological role(s) of this receptor in gnathostomes are not well understood. For mice, MC5R has been implicated in the regulation of secretion by some exocrine glands (Chen et al 1997, van der Kraan et al 1998, Zhang et al 2011, and this receptor may also be involved in the regulation of thermoregulation in mice (Chen et al 1997).…”

Section: Mc5rmentioning

confidence: 99%

60 YEARS OF POMC: Melanocortin receptors: evolution of ligand selectivity for melanocortin peptides

Dores

Liang

Davis

et al. 2016

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

The evolution of the melanocortin receptors (MCRs) is linked to the evolution of adrenocorticotrophic hormone (ACTH), the melanocyte-stimulating hormones (MSHs), and their common precursor pro-opiomelanocortin (POMC). The origin of the MCRs and POMC appears to be grounded in the early radiation of the ancestral protochordates. During the genome duplications that have occurred during the evolution of the chordates, the organization plan for POMC was established, and features that have been retained include, the high conservation of the amino acid sequences of α-MSH and ACTH, and the presence of the HFRW MCR activation motif in all of the melanocortin peptides (i.e. ACTH, α-MSH, β-MSH, γ-MSH, and δ-MSH). For the MCRs, the chordate genome duplication events resulted in the proliferation of paralogous receptor genes, and a divergence in ligand selectivity. While most gnathostome MCRs can be activated by either ACTH or the MSHs, teleost and tetrapod MC2R orthologs can only be activated by ACTH. The appearance of the accessory protein, MRAP1, paralleled the emergence of teleost and tetrapods MC2R ligand selectivity, and the dependence of these orthologs on MRAP1 for trafficking to the plasma membrane. The accessory protein, MRAP2, does not affect MC2R ligand selectivity, but does influence the functionality of MC4R orthologs. In this regard, the roles that these accessory proteins may play in the physiology of the five MCRs (i.e. MC1R, MC2R, MC3R, MC4R, and MC5R) are discussed.

show abstract

“…The MC3-R and MC4-R are for the most part expressed in brain (Butler 2006; Cone 2006; Sutton, et al 2006) but there are reports of MC3-R expression in leukocytes (Getting, et al 2001; Getting et al 2008) and chondrogenic cells (Evans, et al 2004) as well as reports of MC4-R expression in peripheral tissues (Mountjoy, et al 2003; Siljee-Wong 2011). The MC5-R is the most ubiquitous and is highly expressed in exocrine tissues (van der Kraan, et al 1998; Zhang, et al 2011). …”

Section: Introductionmentioning

confidence: 99%

ACTH promotes chondrogenic nodule formation and induces transient elevations in intracellular calcium in rat bone marrow cell cultures via MC2-R signaling

2013

View full text Add to dashboard Cite

Adrenocorticotropic hormone (ACTH) is among the several melanocortin peptide hormones that are derived from proopiomelanocortin (POMC). ACTH has been found to enhance osteogenesis and chondrogenesis. We show that in the presence of dexamethasone, ACTH dose-dependently increases chondrogenic nodule formation in bone marrow stromal cells (BMSC) from the Wystar Kyoto (WKY) rat. The nodules consist of condensed cells highly expressing alkaline phosphatase, Sox9 and type II collagen transcripts, and a proteoglycan rich matrix. Immunoblot analysis of crude membrane fractions was used to determine that these cells express three melanocortin receptors (MC-R); MC2-R, MC3-R and MC5-R, as well as the melanocortin 2-receptor accessory protein (MRAP). To determine which of these receptors mediate ACTH-induced effects, we used MC-R specific peptides and the known agonist profiles of the receptors. Neither α-MSH, a strong agonist of the MC5-R nor γ2-MSH, a strong agonist of the MC3-R, duplicates ACTH effects in rat BMSC. In addition, calcium flux was examined as a mechanism for ACTH action at the MC2-R. Consistent with MC2-R and MRAP expression patterns in the BMSC cultures, ACTH-induced transient increases in intracellular calcium were increased with dexamethasone treatment. Neither α-MSH nor γ2-MSH affected calcium flux. Dexamethasone increased MC2-R and MRAP expression as well as POMC peptide expression and cleavage to increase the production of the lipolytic β-LPH product. Therefore the effects of ACTH in rat BMSC enriched for mesenchymal progenitors are consistent with an MC2-R signaling mechanism and dexamethasone is capable of regulating components of the melanocortin system in these cells.

show abstract

Melanocortin-5 receptor and sebogenesis

Cited by 43 publications

References 58 publications

Role of insulin resistance and diet in acne

Role of insulin resistance and diet in acne

60 YEARS OF POMC: Melanocortin receptors: evolution of ligand selectivity for melanocortin peptides

ACTH promotes chondrogenic nodule formation and induces transient elevations in intracellular calcium in rat bone marrow cell cultures via MC2-R signaling

Contact Info

Product

Resources

About