Effect of Prolactin-Induced Protein on Human Skin: New Insight into the Digestive Action of This Aspartic Peptidase on the Stratum Corneum and Its Induction of Keratinocyte Proliferation

Sugiura, S.; Tazuke, Misao; Ueno, Shoichi; Sugiura, Yasuo; Kato, Ikuo; Miyahira, Yoshimitsu; Yamamoto, Yutaka; Sato, Hiroshi; Udagawa, Jun; Uehara, Masami; Sugiura, Hisashi

doi:10.1038/jid.2014.448

Cited by 6 publications

(4 citation statements)

References 33 publications

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“…Another study demonstrated that PIP is required for cell cycle progression, including the progression through G1 phase, mitosis, and cytokinesis, through regulating genes controlling these processes, such as cyclin D1, cyclin B1, BUB1, and FOXM1 [ 44 ]. Sugiura et al found that PIP could induce the proliferation of epidermal keratinocytes in a human 3-D skin model and speculated that this phenomenon might be caused by an indirect effect of PIP through stratum corneum damage [ 45 ]. Other researchers reported the opposite finding that androgens could increase the expression of PIP and strongly inhibits proliferation of breast cancer cells in an estrogen-sensitive ZR-75-1 cell line [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Prolactin-Induced Protein Promotes Osteogenic Differentiation of Periodontal Ligament Stem Cells

Zhang

Jia

et al. 2021

Med Sci Monit

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Background Periodontal ligament stem cells (PDLSCs) are promising seed cells for bone tissue engineering and periodontal regeneration applications. However, the mechanism underlying the osteogenic differentiation process remains largely unknown. Previous reports showed that prolactin-induced protein (PIP) was upregulated after PDLSCs osteogenic induction. However, few studies have reported on the function of PIP in osteogenic differentiation. The purpose of the present study was to investigate the effect of PIP on osteogenic differentiation of PDLSCs. Material/Methods The expression pattern of PIP during PDLSCs osteogenic differentiation was detected and the effect of each component in the osteogenic induction medium on PIP was also tested by qRT-PCR. Then, the PIP knockdown cells were established using lentivirus. The knockdown efficiency was measured and the proliferation, apoptosis, and osteogenic differentiation ability were examined to determine the functional role of PIP on PDLSCs. Results QRT-PCR showed that PIP was sustainedly upregulated during the osteogenic induction process and the phenomenon was mainly caused by the stimulation of dexamethasone in the induction medium. CCK-8 and flow cytometer showed that knocking down PIP had no influence on proliferation and apoptosis of PDLSCs. ALP staining and activity, Alizarin Red staining, and western blot analysis demonstrated PIP knockdown enhanced the osteogenic differentiation and mineralization of PDLSCs. Conclusions PIP was upregulated after osteogenic induction; however, PIP knockdown promoted PDLSCs osteogenic differentiation. PIP might be a by-product of osteogenic induction, and downregulating of PIP might be a new target in bone tissue engineering applications.

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Section: Discussionmentioning

confidence: 99%

Downregulation of Prolactin-Induced Protein Promotes Osteogenic Differentiation of Periodontal Ligament Stem Cells

Zhang

Jia

et al. 2021

Med Sci Monit

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“…PIP is found in a variety of human secretions, has immunoregulatory functions, and is abundantly expressed in human cancers, especially breast cancer, where it exerts tumor-promoting actions [ 65 ]. A study showed that PIP can damage the skin barrier and induce keratinocyte proliferation [ 66 ]. Annexin A2 (ANXA2) is a member of the annexin family.…”

Section: Discussionmentioning

confidence: 99%

Quantitative proteomics analysis of young and elderly skin with DIA mass spectrometry reveals new skin aging-related proteins

Liu

Wang

et al. 2020

Aging

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Skin aging is a specific manifestation of the physiological aging process that occurs in virtually all organisms. In this study, we used data independent acquisition mass spectrometry to perform a comparative analysis of protein expression in volar forearm skin samples from of 20 healthy young and elderly Chinese individuals. Our quantitative proteomic analysis identified a total of 95 differentially expressed proteins (DEPs) in aged skin compared to young skin. Enrichment analyses of these DEPs (57 upregulated and 38 downregulated proteins) based on the GO, KEGG, and KOG databases revealed functional clusters associated with immunity and inflammation, oxidative stress, biosynthesis and metabolism, proteases, cell proliferation, cell differentiation, and apoptosis. We also found that GAPDH, which was downregulated in aged skin samples, was the top hub gene in a protein-protein interaction network analysis. Some of the DEPs identified herein had been previously correlated with aging of the skin and other organs, while others may represent novel age-related entities. Our non-invasive proteomics analysis of human epidermal proteins may guide future research on skin aging to help develop treatments for age-related skin conditions and rejuvenation.

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“…42 Prolactin-induced protein is an aspartic peptidase found in the epidermis and acrosyrinx of eccrine sweat glands. 66 Application of prolactin-induced protein to a 3D human skin model caused digestion of stratum corneum and epidermal proliferation. Dermcidin, or proteolysis-inducing factor, is a sweat ■ FIGURE 3.…”

Section: Apocrine Gland Variationmentioning

confidence: 99%

Pathophysiology of hidradenitis suppurativa

Hoffman¹,

Ghias²,

Lowes³

2017

Sem Cutan Med Surg

102

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The pathophysiology of hidradenitis suppurativa (HS) is not well understood. Some of our knowledge comes from clinical and epidemiological observations, along with studies of the histopathology and immunohistochemistry of affected skin. More recently, cutaneous molecular studies and transcriptomic analyses have provided additional information regarding inflammatory processes. The chronic cutaneous inflammation, systemic symptoms, and associated comorbidities suggest that HS should be classified as an immune-mediated disease, rather than a primary infectious disease. As such, a proposed integrated disease pathway is presented. At a fundamental level, there appears to be a primary abnormality in the pilosebaceous-apocrine unit, which leads to follicular occlusion, perifollicular cyst development that traps commensal microbes, and rupture into the dermis. This can trigger an exaggerated response of the cutaneous innate immune system. Initially this is an acute event, but ongoing intermittent disease activity can lead to recurrent inflammatory nodules and dermal tunnels. Once underway, the cutaneous inflammation is very difficult to turn off, leading to suppurative inflammation in whole anatomic regions. As the disease progresses, we propose that there is recruitment of the systemic immune system perpetuating the chronic cutaneous inflammatory process. There remains much to be done to understand the pathogenesis and immune signature of this challenging disease.

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Effect of Prolactin-Induced Protein on Human Skin: New Insight into the Digestive Action of This Aspartic Peptidase on the Stratum Corneum and Its Induction of Keratinocyte Proliferation

Cited by 6 publications

References 33 publications

Downregulation of Prolactin-Induced Protein Promotes Osteogenic Differentiation of Periodontal Ligament Stem Cells

Downregulation of Prolactin-Induced Protein Promotes Osteogenic Differentiation of Periodontal Ligament Stem Cells

Quantitative proteomics analysis of young and elderly skin with DIA mass spectrometry reveals new skin aging-related proteins

Pathophysiology of hidradenitis suppurativa

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