Dermal adipose tissue has high plasticity and undergoes reversible dedifferentiation in mice

Zhang, Zhuzhen; Shao, Mengle; Hepler, Chelsea; Zi, Zhenzhen; Zhao, Shangang; An, Yu; Zhu, Yi; Ghaben, Alexandra L.; Wang, May-Yun; Li, Na; Onodera, Toshiharu; Joffin, Nolwenn; Crewe, Clair; Zhu, Qianzheng; Vishvanath, Lavanya; Kumar, Ashwani; Xing, Chao; Wang, Qiong A.; Gautron, Laurent; Deng, Yingfeng; Gordillo, Ruth; Kruglikov, Ilja L.; Kusminski, Christine M.; Gupta, Rana K.; Scherer, Philipp E.

doi:10.1172/jci130239

Cited by 117 publications

(156 citation statements)

References 58 publications

(115 reference statements)

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“…This special fat depot located in the superficial hypodermis and around the distal parts of PSUs demonstrates significant volume oscillations during HF cycle . As we discovered very recently, this effect is connected with repeated de‐ and re‐differentiation processes, which affect 90%‐95% of the adipose cells from dWAT (Figure ) . The de‐differentiation of mature dermal adipocytes in adipocyte‐derived preadipocytes (ADPs) is connected to a dramatic reduction in the cell volumes .…”

Section: Caveolin and Hyperseborrheamentioning

confidence: 84%

“…The main source for cathelicidin in the murine skin is provided by differentiating immature dermal adipocytes . Very recently, we have performed gene expression analysis on highly purified dermal adipocytes and identified Camp gene expression for cathelicidin as a marker for these cells …”

Section: Cav‐1 In Innate Immunitymentioning

confidence: 99%

“…Of note, Cav-1 is required for the uptake of fatty acids through regulation of the fatty acid translocase (FAT/CD36) at the plasma membrane. [74] Since fatty acids are released by mature adipocytes during their de-differentiation into ADPs in the catagen phase and are re-absorbed during re-differentiation of these cells into mature adipocytes in anagen, [13] local autophagy in the skin should demonstrate HF cycle specific variations. Indeed, whole-mount staining of HFs and surrounding dWAT reveals an increased expression of the autophagy marker LC3B during catagen.…”

Section: Av-1 Autophagy and Acnementioning

confidence: 99%

“…Further, local overloading of the skin with free fatty acids causing inflammation can be provided not only by the sebaceous gland. In fact, dermal adipocytes can provide significant local levels of the free fatty acids around the distal end of PSU during their physiological de‐differentiation into adipocyte‐derived preadipocytes (ADPs) in the catagen phase of the hair follicle (HF) cycle …”

Section: Introductionmentioning

confidence: 99%

“…In fact, dermal adipocytes can provide significant local levels of the free fatty acids around the distal end of PSU during their physiological de-differentiation into adipocyte-derived preadipocytes (ADPs) [12] in the catagen phase of the hair follicle (HF) cycle. [13] Transforming growth factor β (TGF-β) is actively produced by human fibroblasts and plays an important role in functioning of sebocytes and keratinocytes. Whereas TGF-β can exist in different isoforms, it appears that only TGF-β1 plays an important role in acne, being strongly upregulated in acne lesions.…”

Section: Introductionmentioning

confidence: 99%

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Caveolin‐1 as a possible target in the treatment for acne

Kruglikov¹,

Scherer

2019

Experimental Dermatology

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Expression of caveolin-1 (Cav-1) is an important pathophysiological factor in acne.Cav-1 strongly interacts with such well-recognized etiopathogenic factors such as hyperseborrhea, follicular hyperkeratinization and pathogenicity of Cutibacterium acnes. Cav-1 is a strong negative regulator of transforming growth factor beta (TGFβ) expression. It acts as a critical determinant of autophagy, which is significantly induced in acne lesions through C. acnes and by absorption of fatty acids. Cav-1 also demonstrates different correlations with the development of innate immunity. We propose that normalization of Cav-1 expression can serve as a target in anti-acne therapy. K E Y W O R D Sacne, autophagy, C. acnes, caveolin, follicular hyperkeratinization, hyperseborrhea, innate immunity, pathophysiology

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Section: Caveolin and Hyperseborrheamentioning

confidence: 84%

Section: Cav‐1 In Innate Immunitymentioning

confidence: 99%

Section: Av-1 Autophagy and Acnementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Caveolin‐1 as a possible target in the treatment for acne

Kruglikov¹,

Scherer

2019

Experimental Dermatology

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Skin aging: Dermal adipocytes metabolically reprogram dermal fibroblasts

Kruglikov¹,

Zhang

Scherer

2021

BioEssays

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Emerging data connects the aging process in dermal fibroblasts with metabolic reprogramming, provided by enhanced fatty acid oxidation and reduced glycolysis. This switch may be caused by a significant expansion of the dermal white adipose tissue (dWAT) layer in aged, hair-covered skin. Dermal adipocytes cycle through dedifferentiation and re-differentiation. As a result, there is a strongly enhanced release of free fatty acids into the extracellular space during the de-differentiation of dermal adipocytes in the catagen phase of the hair follicle cycle. Both caveolin-1 and adiponectin are critical factors influencing these processes. Controlling the expression levels of these two factors also offers the ability to manipulate the metabolic preferences of the different cell types within the microenvironment of the skin, including dermal fibroblasts. Differential expression of adiponectin and caveolin-1 in the various cell types may also be responsible for the cellular metabolic heterogeneity within the cells of the skin.

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Deciphering adipose development: Function, differentiation and regulation

Guo,

Wang,

et al. 2024

Developmental Dynamics

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The overdevelopment of adipose tissues, accompanied by excess lipid accumulation and energy storage, leads to adipose deposition and obesity. With the increasing incidence of obesity in recent years, obesity is becoming a major risk factor for human health, causing various relevant diseases (including hypertension, diabetes, osteoarthritis and cancers). Therefore, it is of significance to antagonize obesity to reduce the risk of obesity‐related diseases. Excess lipid accumulation in adipose tissues is mediated by adipocyte hypertrophy (expansion of pre‐existing adipocytes) or hyperplasia (increase of newly‐formed adipocytes). It is necessary to prevent excessive accumulation of adipose tissues by controlling adipose development. Adipogenesis is exquisitely regulated by many factors in vivo and in vitro, including hormones, cytokines, gender and dietary components. The present review has concluded a comprehensive understanding of adipose development including its origin, classification, distribution, function, differentiation and molecular mechanisms underlying adipogenesis, which may provide potential therapeutic strategies for harnessing obesity without impairing adipose tissue function.

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Dermal adipose tissue has high plasticity and undergoes reversible dedifferentiation in mice

Cited by 117 publications

References 58 publications

Caveolin‐1 as a possible target in the treatment for acne

Caveolin‐1 as a possible target in the treatment for acne

Skin aging: Dermal adipocytes metabolically reprogram dermal fibroblasts

Deciphering adipose development: Function, differentiation and regulation

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