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10.1007/s40620-021-01173-0 http://scihub22266oqcxt.onion/10.1007/s40620-021-01173-0 34626364!8501346!34626364     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\34626364.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Nephrol 2022 ; 35 (3): 735-743 Nephropedia Template TP {{tp|p=34626364|t=2022. Activation of STAT3 signaling pathway in the kidney of COVID-19 patients |pdf=|usr=}}{{34626364}} gab.com Text Activation of STAT3 signaling pathway in the kidney of COVID-19 patients JO: J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=34626364 #FOAvip BACKGROUND: Acute kidney injury is common in patients with COVID-19, however mechanisms of kidney injury remain unclear. Since cytokine storm is likely a cause of AKI and glomerular disease, we investigated the two major transcription factors, STAT3 and NF-kB, which are known to be activated by cytokines. METHODS: This is an observational study of the postmortem kidneys of 50 patients who died with COVID-19 in the Mount Sinai Hospital during the first pandemic surge. All samples were reviewed under light microscopy, electron microscopy, and immunofluorescence by trained renal pathologists. In situ hybridization evaluation for SARS-CoV-2 and immunostaining of transcription factors STAT3 and NF-kB were performed. RESULTS: Consistent with previous findings, acute tubular injury was the major pathological finding, together with global or focal glomerulosclerosis. We were not able to detect SARS-CoV-2 in kidney cells. ACE2 expression was reduced in the tubular cells of patients who died with COVID-19 and did not co-localize with TMPRSS2. SARS-CoV-2 was identified occasionally in the mononuclear cells in the peritubular capillary and interstitium. STAT3 phosphorylation at Tyr705 was increased in 2 cases in the glomeruli and in 3 cases in the tubulointerstitial compartments. Interestingly, STAT3 phosphorylation at Ser727 increased in 9 cases but only in the tubulointerstitial compartment. A significant increase in NF-kB phosphorylation at Ser276 was also found in the tubulointerstitium of the two patients with increased p-STAT3 (Tyr705). CONCLUSIONS: Our findings suggest that, instead of tyrosine phosphorylation, serine phosphorylation of STAT3 is commonly activated in the kidney of patients with COVID-19. Twit Text FOAVip Activation of STAT3 signaling pathway in the kidney of COVID-19 patients ????J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=34626364 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34626364 #FOAvip English Wikipedia <ref>{{Cite pmid|34626364}}</ref> Activation of STAT3 signaling pathway in the kidney of COVID-19 patients #MMPMID34626364 Salem F; Li XZ; Hindi J; Casablanca NM; Zhong F; El Jamal SM; Haroon Al Rasheed MR; Li L; Lee K; Chan L; He JC J Nephrol 2022[Apr]; 35 (3): 735-743 PMID34626364show ga BACKGROUND: Acute kidney injury is common in patients with COVID-19, however mechanisms of kidney injury remain unclear. Since cytokine storm is likely a cause of AKI and glomerular disease, we investigated the two major transcription factors, STAT3 and NF-kB, which are known to be activated by cytokines. METHODS: This is an observational study of the postmortem kidneys of 50 patients who died with COVID-19 in the Mount Sinai Hospital during the first pandemic surge. All samples were reviewed under light microscopy, electron microscopy, and immunofluorescence by trained renal pathologists. In situ hybridization evaluation for SARS-CoV-2 and immunostaining of transcription factors STAT3 and NF-kB were performed. RESULTS: Consistent with previous findings, acute tubular injury was the major pathological finding, together with global or focal glomerulosclerosis. We were not able to detect SARS-CoV-2 in kidney cells. ACE2 expression was reduced in the tubular cells of patients who died with COVID-19 and did not co-localize with TMPRSS2. SARS-CoV-2 was identified occasionally in the mononuclear cells in the peritubular capillary and interstitium. STAT3 phosphorylation at Tyr705 was increased in 2 cases in the glomeruli and in 3 cases in the tubulointerstitial compartments. Interestingly, STAT3 phosphorylation at Ser727 increased in 9 cases but only in the tubulointerstitial compartment. A significant increase in NF-kB phosphorylation at Ser276 was also found in the tubulointerstitium of the two patients with increased p-STAT3 (Tyr705). CONCLUSIONS: Our findings suggest that, instead of tyrosine phosphorylation, serine phosphorylation of STAT3 is commonly activated in the kidney of patients with COVID-19. |*Acute Kidney Injury/diagnosis/pathology[MESH] |*COVID-19/complications[MESH] |Humans[MESH] |Kidney/pathology[MESH] |NF-kappa B[MESH] |SARS-CoV-2[MESH] |STAT3 Transcription Factor[MESH]Activation of STAT3 signaling pathway in the kidney of COVID-19 patien(epmc).pdf DeepDyve Pubget Overpricing