The association of profilin‐1 levels with survival in chronic kidney disease

Ünal, Hilmi Umut; Güçlü, Aydın; Koçyiğit, İsmail; Karaman, Murat; Sağlam, Mutlu; Gezer, Mustafa; Taş, Ahmet; Zararsız, Gökmen; Eyıleten, Tayfun; Aydın, İbrahim; Oğuz, Yusuf; Güngör, Özkan; Yılmaz, Mahmut İlker

doi:10.1111/eci.12839

Cited by 4 publications

(5 citation statements)

References 34 publications

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“…Therefore, myosin is diffusely activated in stress fibers, extending to focal adhesions, immobilizing the fibroblast, and promoting myofibroblast differentiation in fibrotic lung progression [23][24][25]. A clinical research reported that Pfn1 is highly expressed in endothelial cells and in the serum of patients with decreased eGFR [11]. Our study also observed increased Pfn1 expression in TH1 cells treated with P-cresol.…”

Section: Discussionsupporting

confidence: 71%

“…Pfn1 regulates cellular homeostasis and maintains cytoskeletal structure. However, previous clinical studies verified that Pfn1 is highly expressed in endothelial cells and in the serum of CKD patients with decreased eGFR [11]. These results indicate that, in CKD patients, the overexpression of Pfn1 disrupts the homeostasis of actin dynamics and increase F-actin in renal proximal tubule epithelial cells.…”

Section: Ivyspringmentioning

confidence: 83%

“…Previous clinical studies reported that the expression of Pfn1 is highly increased in the serum of CKD patients with a low recovery rate [11]. We assumed that renal fibrosis could be inhibited by downregulating the upstream regulator of Pfn1.…”

Section: Profilin-1 Is Increased In the Ckd Mouse Modelmentioning

confidence: 96%

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Knockdown of CK2α reduces P-cresol-induced fibrosis in human renal proximal tubule epithelial cells via the downregulation of profilin-1

Yoon¹,

Go²,

Yun³

et al. 2020

Int. J. Med. Sci.

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Renal fibrosis is one of the main causes of chronic kidney disease. Many studies have focused on fibroblasts and myofibroblasts involved in renal fibrogenesis. Recently, several studies have reported that renal proximal tubule epithelial cells are possible initiators of renal fibrosis. However, the mechanism through which cells induce renal fibrosis is poorly understood. In this study, we found that CK2α induces fibrosis in renal proximal tubule epithelial cells (TH1) by regulating the expression of profilin-1 (Pfn1). CKD mouse model and TH1 cells treated with P-cresol also showed an increased level of Pfn1. The knockdown of CK2α suppressed fibrosis in TH1 cells via the downregulation of Pfn1. In particular, CK2α knockdown inhibited the expression of stress fibers and fibrosis-related proteins in P-cresol-treated TH1 cells. Furthermore, the knockdown of CK2α inhibited mitochondrial dysfunction and restored cellular senescence and cell cycle in P-cresol-treated TH1 cells. These results indicate that CK2α induces renal fibrosis through Pfn1, which makes CK2α a key target molecule in the treatment of fibrosis related to chronic kidney disease.

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Section: Discussionsupporting

confidence: 71%

Section: Ivyspringmentioning

confidence: 83%

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Knockdown of CK2α reduces P-cresol-induced fibrosis in human renal proximal tubule epithelial cells via the downregulation of profilin-1

Yoon¹,

Go²,

Yun³

et al. 2020

Int. J. Med. Sci.

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“…Profilin 1 played an important role in regulation of actin polymerization and cytoskeleton remodeling ( Stritt et al, 2018 ). Serum profilin 1 was independently associated with endothelial dysfunction, cardiovascular events and survival in patients with chronic kidney disease ( Eroglu et al, 2017 ; Li X. et al, 2018 ). Mutations in profilin 1 led to familiar amyotrophic lateral sclerosis ( Daigle et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Protein Tyrosine Phosphatase Receptor S Acts as a Metastatic Suppressor in Malignant Peripheral Nerve Sheath Tumor via Profilin 1-Induced Epithelial-Mesenchymal Transition

Ren

Cui

et al. 2020

Front. Cell Dev. Biol.

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Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas with over half of cases developed in the context of neurofibromatosis type 1. Surgical resection is the only effective therapy for MPNST. The prognosis is very dismal once recurrence or metastasis occurs. Epithelial-mesenchymal transition (EMT) is a key process of recurrence and metastasis involving reorganizations of the actin cytoskeleton and actin-binding proteins (ABP) play a non-negligible role. Protein tyrosine phosphatase receptor S (PTPRS), a tumor suppressor previously reported in colorectal cancer, hepatocellular carcinoma and head and neck cancer, is thought to mediate cell migration and invasion by downregulation of EMT. However, its role in MPNST remains unknown. In the present study, by using tissue microarray we demonstrated low expression of PTPRS was related to poor prognosis in MPNST. Knockdown of PTPRS in MPNST cell lines increased migration/invasion and EMT processes were induced with increased N-cadherin and decreased E-cadherin, which indicated PTPRS may serve as a tumor suppressor in MPNST. In addition, we tested all EMT related ABP and found profilin 1 was significantly elevated in PTPRS downregulated MPNST cell lines. As a member of actin-binding proteins, profilins are regulators of actin polymerization and contribute to cell motility and invasion, which have been reported to be responsible for EMT. Moreover, results showed that downregulation of profilin 1 could restore the EMT processes caused by PTPRS downregulation in vitro and in vivo . Furthermore, high expression of profilin 1 was significantly associated with dismal prognosis. These results highlighted PTPRS served as a potential tumor suppressor in the recurrence and metastasis of MPNST via profilin 1 induced EMT processes and it might provide potential targets for future clinical therapeutics.

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“…A PNF1 atua como um regulador complexo de montagem de actina monomérica (G-actina) em filamentos (F-actina) (Bubb et al 2003;Pollard and Borisy 2003). Esta proteína foi encontrada aumentada na urina de pacientes com doença renal policística e a PNF1 sérica foi independentemente associada com disfunção endotelial, eventos cardiovasculares e sobrevida de pacientes com DRC (Bakun et al 2012;Eroglu et al 2017). A PNF1 já foi nitrada in vitro e verificado que a nitração inibe a sua propriedade sequestradora de actina, reduzindo a concentração de monômero de actina ligada a ela (Kasina et al 2005).…”

Section: )unclassified

Perfil proteômico da lesão renal aguda induzida por isquemia e reperfusão

Malagrino¹

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The association of profilin‐1 levels with survival in chronic kidney disease

Abstract: This is the first study that demonstrates the serum profilin-1 is independently associated with endothelial dysfunction, cardiovascular events and survival in patients with CKD.

Cited by 4 publications

References 34 publications

Knockdown of CK2α reduces P-cresol-induced fibrosis in human renal proximal tubule epithelial cells via the downregulation of profilin-1

Knockdown of CK2α reduces P-cresol-induced fibrosis in human renal proximal tubule epithelial cells via the downregulation of profilin-1

Protein Tyrosine Phosphatase Receptor S Acts as a Metastatic Suppressor in Malignant Peripheral Nerve Sheath Tumor via Profilin 1-Induced Epithelial-Mesenchymal Transition

Perfil proteômico da lesão renal aguda induzida por isquemia e reperfusão

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