PPL

Last update 08 May 2025

Basic Info

Synonyms

190 kDa paraneoplastic pemphigus antigen, 195 kDa cornified envelope precursor protein, KIAA0568

+ [2]

Introduction

Component of the cornified envelope of keratinocytes. May link the cornified envelope to desmosomes and intermediate filaments. May act as a localization signal in PKB/AKT-mediated signaling.

100 Clinical Results associated with PPL

100 Translational Medicine associated with PPL

0 Patents (Medical) associated with PPL

457

Literatures (Medical) associated with PPL

01 Jan 2025·Research and Practice in Thrombosis and Haemostasis

Effect of plasma levels of factor VIII according to procoagulant phospholipids on the risk of future venous thromboembolism

Article

Author: Latysheva, Nadezhda ; Morelli, Vânia M ; Hansen, John-Bjarne ; Hansen, Ellen-Sofie ; Aukrust, Pål ; Snir, Omri ; Edvardsen, Magnus S ; Ueland, Thor

BackgroundA high level of plasma coagulation factor (F)VIII is an established and likely causal risk factor for venous thromboembolism (VTE). Procoagulant phospholipids (PPLs) facilitate FVIII activity in coagulation.ObjectivesTo assess the association between plasma levels of FVIII and risk of future VTE according to PPL clotting time (PPL_CT), an inverse surrogate measure of plasma PPL activity.MethodsA population-based nested case-control study comprising 278 incident VTE cases and 593 randomly selected age- and sex-matched controls were derived from the Tromsø cohort. Exposures were determined from data collected at the cohort baseline. Logistic regression was used to estimate odds ratios (ORs) with 95% CIs for VTE across tertiles of FVIII and PPL_CT.ResultsHigh (tertile 3) vs low (tertile 1) FVIII antigen levels resulted in an age- and sex-adjusted OR of 1.53 (95% CI, 0.78-3.00) in those with high PPL_CT (low PPL activity), while the corresponding OR for those with low PPL_CT (high PPL activity) was 1.88 (95% CI, 0.96-3.66). In the biological interaction analysis, participants with both high FVIII and PPL activity had an OR of 1.86 (95% CI, 0.97-3.57) compared with those with low FVIII and PPL activity. In the joint exposure group, 10% (95% CI, -55% to 75%) of VTEs could be attributable to the interaction between FVIII and PPL activity. Results remained similar after further adjustment for body mass index, C-reactive protein, arterial cardiovascular disease, and cancer.ConclusionThe effect of high FVIII levels on VTE risk was particularly augmented in those with high PPL activity, suggesting that the effect of FVIII on VTE risk might be partially dependent on PPL activity.

01 Jan 2025·Cellular and Molecular Gastroenterology and Hepatology

Periplakin Attenuates Liver Fibrosis via Reprogramming CD44Low Cells into CD44High Liver Progenitor Cells

Article

Author: Hu, Yunyi ; Zhao, Siyu ; Xu, Meiyining ; Shen, Jia ; Liu, Xianzhi ; Zhang, Lichao ; Wang, Lifu F ; Wu, Zhongdao ; Sun, Xi ; Liu, Shurui ; Chen, Zebin ; Jiang, Kefeng ; Xiong, Zhiyong

BACKGROUND & AIMSLiver progenitor cells (LPCs) contribute significantly to the restoration of injured liver parenchyma and promote liver regeneration, thereby ameliorating liver fibrosis. However, the mechanism of the derivation of LPCs remains poorly understood.METHODSWe first examined the expression of periplakin (PPL) in patients and mouse models with liver fibrosis. Adenovirus overexpressing PPL was injected into the tail vein of mouse models to detect the regulatory effect of PPL on liver fibrosis. Single-cell sequencing explored how PPL influences liver fibrosis progression. Additionally, PPL⁺CD44^Low cells and PPL⁺CD44^High LPCs were transplanted into 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced mouse models to assess their therapeutic efficacy in treating liver fibrosis.RESULTSThe expression of PPL is upregulated in fibrotic livers in human and mouse models of liver fibrosis. Functionally, we found that PPL overexpression significantly attenuated liver fibrosis. Mechanistically, PPL was specifically expressed in LPCs and promoted LPC expansion. Moreover, we observed that PPL⁺ cells could be categorized into PPL⁺CD44^Low and PPL⁺CD44^High subsets, and PPL⁺CD44^Low cells were found to redifferentiate into PPL⁺CD44^High LPCs during liver fibrosis. Furthermore, transplantation of PPL⁺CD44^High LPCs notably suppressed liver fibrosis.CONCLUSIONSThese findings demonstrate that PPL⁺CD44^Low cells can be reprogrammed into PPL⁺CD44^High LPCs, which ameliorate liver fibrosis, suggesting a potential application of PPL for the treatment of liver fibrosis.

14 Nov 2024·Journal of Medicinal Chemistry

Targeting Periplakin of Novel Benzenesulfonamides as Highly Selective Agonists for the Treatment of Vitiligo

Article

Author: Wang, Feifei ; Lai, Yifan ; Zha, Xiaoming ; Shang, Jing ; Li, Panpan ; Li, Liqiang ; Yan, Qiuming ; Zhong, Hui ; Zhang, Xin ; Xia, Yu

Vitiligo is the most common cause of depigmentation worldwide, with immunosuppressive treatments often being inefficient and prone to recurrence, making it essential to identify new therapeutic targets. Periplakin (PPL) has been identified and confirmed as a key factor in vitiligo-related depigmentation. Based on this, a series of selective PPL agonists, specifically benzenesulfonamides, have been developed. Among these, compound I-3 exhibits superior efficacy compared to ruxolitinib, the only FDA-approved treatment for vitiligo. I-3 has been shown to increase cAMP levels by regulating PPL, which enhances MITF expression, a key transcription factor in melanin biosynthesis. Additionally, I-3 promotes melanin production by regulating tryptophan metabolism. In summary, PPL is a promising drug target, and I-3 has strong potential for future treatment of vitiligo due to its high selectivity and favorable druggability.

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