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10.3389/fimmu.2018.00619 http://scihub22266oqcxt.onion/10.3389/fimmu.2018.00619 C5884871!5884871 !29651290     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 300.79999999999995 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\29651290 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Immunol 2018 ; 9 (ä): 619 Nephropedia Template TP {{tp|p=29651290 |t=2018. Anti-Transforming Growth Factor ? IgG Elicits a Dual Effect on Calcium Oxalate Crystallization and Progressive Nephrocalcinosis-Related Chronic Kidney Disease |pdf=|usr=}}{{29651290 }} gab.com Text Anti-Transforming Growth Factor IgG Elicits a Dual Effect on Calcium Oxalate Crystallization and Progressive Nephrocalcinosis-Related Chronic Kidney Disease JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29651290 #FOAvip Crystallopathies are a heterogeneous group of diseases caused by intrinsic or environmental microparticles or crystals, promoting tissue inflammation and scarring. Certain proteins interfere with crystal formation and growth, e.g., with intrarenal calcium oxalate (CaOx) crystal formation, a common cause of kidney stone disease or nephrocalcinosis-related chronic kidney disease (CKD). We hypothesized that immunoglobulins can modulate CaOx microcrystal formation and crystal growth and that therefore, biological IgG-based drugs designed to specifically target disease modifying proteins would elicit a dual effect on the outcome of CaOx-related crystallopathies. Indeed, both the anti-transforming growth factor (TGF)? IgG and control IgG1 antibody impaired CaOx crystallization in vitro, and decreased intrarenal CaOx crystal deposition and subsequent CKD in mice on an oxalate-rich diet compared to oxalate-fed control mice. However, the TGF?-specific IgG antibody showed nephroprotective effects beyond those of control IgG1 and substantially reduced interstitial fibrosis as indicated by magnetic resonance imaging, silver and ?-smooth muscle actin staining, RT-qPCR, and flow cytometry for pro-fibrotic macrophages. Suppressing interstitial fibrosis slowed the decline of glomerular filtration rate (GFR) compared to treatment with control IgG1 [slope of m?=?-8.9 vs. m?=?-14.5??l/min/100?g body weight (BW)/day, ??=?38.3%], an increased GFR at the end of the study (120.4 vs. 42.6??l/min/100?g BW, ??=?64.6%), and prolonged end stage renal disease (ESRD)-free renal survival by 10?days (??=?38.5%). Delayed onset of anti-TGF? IgG from day 7 was no longer effective. Our results suggest that biological drugs can elicit dual therapeutic effects on intrinsic crystallopathies, such as anti-TGF? IgG antibody treatment inhibits CaOx crystallization as well as interstitial fibrosis in nephrocalcinosis-related CKD. Twit Text FOAVip Anti-Transforming Growth Factor IgG Elicits a Dual Effect on Calcium Oxalate Crystallization and Progressive Nephrocalcinosis-Related Chronic Kidney Disease ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29651290 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29651290 #FOAvip English Wikipedia <ref>{{Cite pmid|29651290 }}</ref> Anti-Transforming Growth Factor ? IgG Elicits a Dual Effect on Calcium Oxalate Crystallization and Progressive Nephrocalcinosis-Related Chronic Kidney Disease #MMPMID29651290 Steiger S ; Grill JF ; Ma Q ; Bäuerle T ; Jordan J ; Smolle M ; Böhland C ; Lech M ; Anders HJ Front Immunol 2018[]; 9 (ä): 619 PMID29651290 show ga Crystallopathies are a heterogeneous group of diseases caused by intrinsic or environmental microparticles or crystals, promoting tissue inflammation and scarring. Certain proteins interfere with crystal formation and growth, e.g., with intrarenal calcium oxalate (CaOx) crystal formation, a common cause of kidney stone disease or nephrocalcinosis-related chronic kidney disease (CKD). We hypothesized that immunoglobulins can modulate CaOx microcrystal formation and crystal growth and that therefore, biological IgG-based drugs designed to specifically target disease modifying proteins would elicit a dual effect on the outcome of CaOx-related crystallopathies. Indeed, both the anti-transforming growth factor (TGF)? IgG and control IgG1 antibody impaired CaOx crystallization in vitro, and decreased intrarenal CaOx crystal deposition and subsequent CKD in mice on an oxalate-rich diet compared to oxalate-fed control mice. However, the TGF?-specific IgG antibody showed nephroprotective effects beyond those of control IgG1 and substantially reduced interstitial fibrosis as indicated by magnetic resonance imaging, silver and ?-smooth muscle actin staining, RT-qPCR, and flow cytometry for pro-fibrotic macrophages. Suppressing interstitial fibrosis slowed the decline of glomerular filtration rate (GFR) compared to treatment with control IgG1 [slope of m?=?-8.9 vs. m?=?-14.5??l/min/100?g body weight (BW)/day, ??=?38.3%], an increased GFR at the end of the study (120.4 vs. 42.6??l/min/100?g BW, ??=?64.6%), and prolonged end stage renal disease (ESRD)-free renal survival by 10?days (??=?38.5%). Delayed onset of anti-TGF? IgG from day 7 was no longer effective. Our results suggest that biological drugs can elicit dual therapeutic effects on intrinsic crystallopathies, such as anti-TGF? IgG antibody treatment inhibits CaOx crystallization as well as interstitial fibrosis in nephrocalcinosis-related CKD. |Animals [MESH] |Calcium Oxalate/*chemistry [MESH] |Crystallization [MESH] |Diet [MESH] |Disease Models, Animal [MESH] |Fibrosis [MESH] |Glomerular Filtration Rate/*drug effects [MESH] |Humans [MESH] |Immunoglobulin G/*therapeutic use [MESH] |Kidney/*metabolism/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Nephrocalcinosis/*therapy [MESH] |Oxalates/adverse effects [MESH] |Renal Insufficiency, Chronic/*therapy [MESH]Anti-Transforming Growth Factor ? IgG Elicits a Dual Effect on Calcium(epmc).pdf DeepDyve Pubget Overpricing