oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4

Chen, Yuan; Wang, Zhiyi; Li, Qian; Yu, Lichun; Zhu, Yanji; Wang, Jing; Sun, Song

doi:10.3892/mmr.2020.11292

Cited by 5 publications

(3 citation statements)

References 40 publications

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“…The sequences of the CXCL16 shRNA and ERK1/2 shRNA were amplified and inserted into pLKO.1-TRC control (pLKO.1) to generate recombinant plasmid for lentiviral vector production. The construction of recombinant plasmid was as previously described ( 24 ). Briefly, the sequences of shCXCL16 and shERK1/2 were amplified and inserted into pLKO.1 to generate recombinant pLKO.1-shCXCL16 and pLKO.1-ERK1/2 for lentivirus production.…”

Section: Methodsmentioning

confidence: 99%

CXCL16/ERK1/2 pathway regulates human podocytes growth, migration, apoptosis and epithelial mesenchymal transition

Chen

Wang

et al. 2022

Mol Med Rep

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Primary nephrotic syndrome (PNS) is the commonest glomerular disease affecting children. Previous studies have confirmed that CXC motif chemokine ligand 16 (CXCL16) is involved in the pathogenesis of PNS. However, the exact mechanisms underlying the pathogenesis of PNS remain to be elucidated. Thus, the present study aimed to elucidate the role of CXCL16 in PNS. It was found that the expression of CXCL16 and extracellular signal-regulated kinases 1 and 2 (ERK1/2) were significantly increased in clinical PNS renal tissues using reverse transcription-quantitative PCR, western blot analysis and immunohistochemistry. Lentivirus overexpression or short hairpin RNA vector was used to induce the overexpression or knockdown of CXCL16 in podocytes, respectively. Overexpression of CXCL16 in podocytes could decrease the cell proliferation and increase the migration and apoptosis, whereas CXCL16 knockdown increased cell proliferation and decreased cell migration and apoptosis. Results of the present study further demonstrated that ERK2 protein expression was regulated by CXCL16. The knockdown of ERK2 expression reversed the effects of CXCL16 on the proliferation, apoptosis, migration and epithelial mesenchymal transition (EMT) of podocytes. Collectively, the findings of the present study highlighted that the CXCL16/ERK1/2 pathway regulates the growth, migration, apoptosis and EMT of human podocytes.

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Section: Methodsmentioning

confidence: 99%

CXCL16/ERK1/2 pathway regulates human podocytes growth, migration, apoptosis and epithelial mesenchymal transition

Chen

Wang

et al. 2022

Mol Med Rep

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“…10D) indicating a potential change in this complex's higher order structure. To our knowledge, the effect of atherosclerosis on ACTN4 has yet to be demonstrated, although exposure of oxidised LDLs (oxLDLs) to podocytes was recently shown to significantly enhance podocyte migration by increasing ACTN4 expression [109]. As a major crosslinker of actin, changes in ACTN4 are associated to alterations in cell motility and migration [110].…”

Section: Sex-conserved and -Unique Differences Identified Within Protein Structures From Human Atherosclerotic Plaquementioning

confidence: 99%

Peptide location fingerprinting identifies species- and tissue-conserved structural remodelling of proteins as a consequence of ageing and disease

Eckersley

Ozols

Chen

et al. 2022

Preprint

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Extracellular matrix (ECM) in the intervertebral disc (IVD), lung and artery are thought to undergo the age-dependant accumulation of damage by chronic exposure to mechanisms such as reactive oxygen species, proteases and glycation. It is unknown whether this damage accumulation is species-dependant (via differing lifespans and hence cumulative exposures) or whether it can influence the progression of age-related diseases such as atherosclerosis. Peptide location fingerprinting (PLF) is a new proteomic analysis method, capable of the non-targeted identification of structure-associated changes within proteins. Here we applied PLF to publicly available ageing human IVD (outer annulus fibrosus), ageing mouse lung and human arterial atherosclerosis datasets and identified novel target proteins alongside common age-associated differences within protein structures which were conserved between tissue regions, organs, sexes and species and in age-related disease. We identify peptide yield differences across protein structures which coincide with biological regions, potentially reflecting the functional consequences of ageing or atherosclerosis for macromolecular assemblies (collagen VI and fibrin), enzyme/inhibitor activity (cathepsin B and alpha-2 macroglobulin), activation states (complement C3 and thrombin) and interaction states (laminins, perlecan, fibronectin, filamin-A, collagen XIV and apolipoprotein-B). Furthermore, we show that alpha-2 macroglobulin, prothrombin, collagen XIV and apolipoprotein-B all exhibit possible shared structural consequences in IVD ageing and arterial atherosclerosis, providing novel links between an age-related disease and intrinsic ageing. Crucially, we also demonstrate that fibronectin, laminin beta chains and filamin-A all exhibit conserved age-associated structural differences between mouse lung and human IVD, providing evidence that ECM, and their associating proteins, may be subjected to potentially similar mechanisms or consequences of ageing across species, irrespective of differences in lifespan and tissue function.

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“…CXCL16 is a scavenger receptor, and its release mediates the uptake of oxLDL to induce reactive oxygen species and fibronectin in podocytes [45]. Another study revealed that ADAM10-mediated CXCL16 release modulated the actin cytoskeleton, as well as promoted podocyte migration [46]. Notably, ADAM10 has been identified as the major regulator for Notch signaling, which takes part in the development of glomerular disease.…”

Section: Podocytesmentioning

confidence: 99%

ADAMs family in kidney physiology and pathology

et al. 2021

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A disintegrin and metalloproteinases (ADAMs) family are proteolytic transmembrane proteases that modulate diverse cell functions and coordinate intercellular communication. ADAMs are responsible for regulating cell proliferation, differentiation, migration, and organ morphogenesis in kidney development. Abnormally activated ADAMs drive inflammation and fibrosis in response to kidney diseases such as acute kidney injury, diabetic kidney disease, polycystic kidney disease, and chronic allograft nephropathy. ADAM10 and ADAM17, known as the most characterized members of ADAMs, are extensively investigated in kidney diseases. Notably, ADAM proteases have the potential to be targets for developing novel treatment approaches in kidney diseases.

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oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4

Cited by 5 publications

References 40 publications

CXCL16/ERK1/2 pathway regulates human podocytes growth, migration, apoptosis and epithelial mesenchymal transition

CXCL16/ERK1/2 pathway regulates human podocytes growth, migration, apoptosis and epithelial mesenchymal transition

Peptide location fingerprinting identifies species- and tissue-conserved structural remodelling of proteins as a consequence of ageing and disease

ADAMs family in kidney physiology and pathology

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