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Article ; Online: 2007 Young Investigator Award: TRP'ing into a new era for glomerular disease.

Winn, Michelle P

Journal of the American Society of Nephrology : JASN

2008 Volume 19, Issue 6, Page(s) 1071–1075

Abstract: FSGS is a pathologic lesion that frequently causes the nephrotic syndrome and ensuing renal failure. The cause remains unknown in the majority of individuals; however, in the past two decades, rare familial forms have been identified. It has been ... ...

Abstract	FSGS is a pathologic lesion that frequently causes the nephrotic syndrome and ensuing renal failure. The cause remains unknown in the majority of individuals; however, in the past two decades, rare familial forms have been identified. It has been suggested that known genetic causes of the hereditary form of this disease account for upwards of 18% of cases. Mutations in five genes have been found to cause inherited nephrotic syndromes and FSGS. In this article, I discuss the phenotypic characteristics of hereditary FSGS and the transient receptor potential cation channel 6 (TRPC6) protein, which is the genetic impetus for an autosomal dominant form of FSGS. The TRP channels have been implicated in varied biologic functions such as mechanosensation, ion homeostasis, cell growth, and phospholipase C-dependent calcium entry into cells. The mutated ion channel causes an increase in calcium transients. Current evidence also suggests that blocking TRPC6 channels may be of therapeutic benefit in idiopathic FSGS, a disease with a generally poor prognosis. Preliminary experiments reveal that the commonly used immunosuppressive agent FK-506 can inhibit TRPC6 activity in vivo. This creates the intriguing possibility that blocking TRPC6 channels within the podocyte may translate into long-lasting clinical benefits in patients with FSGS.
MeSH term(s)	Awards and Prizes ; Glomerulosclerosis, Focal Segmental/genetics ; Humans ; Mutation ; Pedigree ; TRPC Cation Channels/genetics ; TRPC6 Cation Channel
Chemical Substances	TRPC Cation Channels ; TRPC6 Cation Channel ; TRPC6 protein, human
Language	English
Publishing date	2008-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2007121292
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Article ; Online: Metabolic obesity phenotypes and obesity-related cancer risk in the National Health and Nutrition Examination Survey.

Winn, Maci / Karra, Prasoona / Freisling, Heinz / Gunter, Marc J / Haaland, Benjamin / Litchman, Michelle L / Doherty, Jennifer A / Playdon, Mary C / Hardikar, Sheetal

Endocrinology, diabetes & metabolism

2023 Volume 6, Issue 4, Page(s) e433

Abstract: Introduction: Body mass index (BMI) fails to identify up to one-third of normal weight individuals with metabolic dysfunction who may be at increased risk of obesity-related cancer (ORC). Metabolic obesity phenotypes, an alternate metric to assess ... ...

Abstract	Introduction: Body mass index (BMI) fails to identify up to one-third of normal weight individuals with metabolic dysfunction who may be at increased risk of obesity-related cancer (ORC). Metabolic obesity phenotypes, an alternate metric to assess metabolic dysfunction with or without obesity, were evaluated for association with ORC risk. Methods: National Health and Nutrition Examination Survey participants from 1999 to 2018 (N = 19,500) were categorized into phenotypes according to the metabolic syndrome (MetS) criteria and BMI: metabolically healthy normal weight (MHNW), metabolically unhealthy normal weight (MUNW), metabolically healthy overweight/obese (MHO) and metabolically unhealthy overweight/obese (MUO). Adjusted multivariable logistic regression models were used to evaluate associations with ORC. Results: With metabolic dysfunction defined as ≥1 MetS criteria, ORC cases (n = 528) had higher proportions of MUNW (28.2% vs. 17.4%) and MUO (62.6% vs. 60.9%) phenotypes than cancer-free individuals (n = 18,972). Compared with MHNW participants, MUNW participants had a 2.2-times higher ORC risk [OR (95%CI) = 2.21 (1.27-3.85)]. MHO and MUO participants demonstrated a 43% and 56% increased ORC risk, respectively, compared to MHNW, but these did not reach statistical significance [OR (95% CI) = 1.43 (0.46-4.42), 1.56 (0.91-2.67), respectively]. Hyperglycaemia, hypertension and central obesity were all independently associated with higher ORC risk compared to MHNW. Conclusions: MUNW participants have a higher risk of ORC than other abnormal phenotypes, compared with MHNW participants. Incorporating metabolic health measures in addition to assessing BMI may improve ORC risk stratification. Further research on the relationship between metabolic dysfunction and ORC is warranted.
MeSH term(s)	Humans ; Overweight ; Nutrition Surveys ; Obesity/complications ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/etiology ; Metabolic Syndrome/diagnosis ; Phenotype ; Neoplasms/epidemiology ; Neoplasms/etiology
Language	English
Publishing date	2023-06-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2398-9238
ISSN (online)	2398-9238
DOI	10.1002/edm2.433
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Article ; Online: Evaluation of a Rapid Fungal Detection Panel for Identification of Candidemia at an Academic Medical Center.

Bomkamp, John P / Sulaiman, Rand / Hartwell, Jennifer L / Desai, Armisha / Winn, Vera C / Wrin, Justin / Kussin, Michelle L / Hiles, Jon J

Journal of clinical microbiology

2020 Volume 58, Issue 3

Abstract: This study was conducted to assess the utility of the T2Candida panel across an academic health center and identify potential areas for diagnostic optimization. A retrospective chart review was conducted on patients with a T2Candida panel and mycolytic/ ... ...

Abstract	This study was conducted to assess the utility of the T2Candida panel across an academic health center and identify potential areas for diagnostic optimization. A retrospective chart review was conducted on patients with a T2Candida panel and mycolytic/fungal (myco/f lytic) blood culture collected simultaneously during hospitalizations from February 2017 to March 2018. The primary outcome of this study was to determine the sensitivity, specificity, and positive and negative predictive values of the panel compared to myco/f lytic blood culture. Secondary outcomes included
MeSH term(s)	Academic Medical Centers ; Candida ; Candidemia/diagnosis ; Candidemia/drug therapy ; Humans ; Micafungin ; Retrospective Studies
Chemical Substances	Micafungin (R10H71BSWG)
Language	English
Publishing date	2020-02-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	390499-4
ISSN	1098-660X ; 0095-1137
ISSN (online)	1098-660X
ISSN	0095-1137
DOI	10.1128/JCM.01408-19
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Article ; Online: TORCing up the importance of calcium signaling.

Lavin, Peter J / Winn, Michelle P

Journal of the American Society of Nephrology : JASN

2011 Volume 22, Issue 8, Page(s) 1391–1393

MeSH term(s)	Animals ; Calcium/metabolism ; Calcium Signaling ; Disease Models, Animal ; Glomerular Filtration Rate ; Humans ; Kidney Diseases/metabolism ; Kidney Glomerulus/metabolism ; Models, Biological ; Mutation ; Rats ; Signal Transduction ; Sirolimus/pharmacology ; Transcription Factors/genetics
Chemical Substances	CRTC1 protein, human ; Transcription Factors ; Calcium (SY7Q814VUP) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2011-08
Publishing country	United States
Document type	Editorial
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2011060595
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Article: Approach to the evaluation of heritable diseases and update on familial focal segmental glomerulosclerosis.

Winn, Michelle P

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2003 Volume 18 Suppl 6, Page(s) vi14–20

Abstract: Focal segmental glomerulosclerosis (FSGS) is a pathological entity that is a significant cause of morbidity and mortality throughout the world. It is also a significant cause of end-stage renal disease (ESRD). Glomerular disease is the third leading ... ...

Abstract	Focal segmental glomerulosclerosis (FSGS) is a pathological entity that is a significant cause of morbidity and mortality throughout the world. It is also a significant cause of end-stage renal disease (ESRD). Glomerular disease is the third leading cause of ESRD, and FSGS comprises a significant proportion of this subgroup. Up to 20% of individuals with ESRD have FSGS. It has been reported in patients from varied ethnic backgrounds including individuals who are of Spanish, North American, North European and African descent. The diagnosis of FSGS is based on renal pathology and requires the presence of areas of glomerular sclerosis and tuft collapse that are both focal and segmental. The clinical hallmarks of FSGS include proteinuria, nephrotic syndrome and, frequently, the progressive loss of renal function. At present, there are no consistently reliable treatments for FSGS and response rates to available treatments have been estimated at <30-50%. FSGS has been characterized previously as having primary (idiopathic), secondary and familial forms. In the latter category, both autosomal recessive and dominant inheritance patterns have been reported. Advances in molecular genetics technology and mapping, including high-throughput genotyping for genomic screening, provide powerful tools for the analysis of renal diseases. Genes associated with many familial renal disorders that lead to ESRD have been isolated; these include Alport's nephropathy, familial juvenile nephronophthisis and adult polycystic disease. Recently, the genetic mutation (ACTN4) causing a form of autosomal dominant FSGS (ACTN4) and congenital nephrotic syndromes (NPHS2) have been described. The existence of hereditary forms of FSGS permits the use of molecular genetics techniques to study the pathogenesis of this disorder.
MeSH term(s)	Genetic Diseases, Inborn/genetics ; Glomerulosclerosis, Focal Segmental/genetics ; Humans
Language	English
Publishing date	2003-05-16
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfg1070
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Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 329: Show issues

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Article: Not all in the family: mutations of podocin in sporadic steroid-resistant nephrotic syndrome.

Winn, Michelle P

Journal of the American Society of Nephrology : JASN

2001 Volume 13, Issue 2, Page(s) 577–579

MeSH term(s)	Drug Resistance ; Humans ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins/genetics ; Mutation/physiology ; Nephrotic Syndrome/genetics ; Nephrotic Syndrome/physiopathology ; Steroids/therapeutic use
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; NPHS2 protein ; Steroids
Language	English
Publishing date	2001-10-30
Publishing country	United States
Document type	Comment ; Editorial ; Review
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.V132577
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Article ; Online: Genetic testing in nephrotic syndrome--challenges and opportunities.

Gbadegesin, Rasheed A / Winn, Michelle P / Smoyer, William E

Nature reviews. Nephrology

2013 Volume 9, Issue 3, Page(s) 179–184

Abstract: Monogenic nephrotic syndrome (nephrotic syndrome caused by a single gene defect) is responsible for only a small percentage of cases of nephrotic syndrome, but information from studies of the unique cohort of patients with this form of the disease has ... ...

Abstract	Monogenic nephrotic syndrome (nephrotic syndrome caused by a single gene defect) is responsible for only a small percentage of cases of nephrotic syndrome, but information from studies of the unique cohort of patients with this form of the disease has dramatically improved our understanding of the disease pathogenesis. The use of genetic testing in the management of children and adults with nephrotic syndrome poses unique challenges for clinicians in terms of who to test and how to use the information obtained from testing in the clinical setting. In our view, not enough data exist at present to justify the routine genetic testing of all patients with nephrotic syndrome. Testing is warranted, however, in patients with congenital nephrotic syndrome (onset at 0-3 months), infantile nephrotic syndrome (onset at 3-12 months), a family history of nephrotic syndrome, and those in whom nephrotic syndrome is associated with other congenital malformations. The family and/or the patient should be given complete and unbiased information on the potential benefits and risks associated with therapy, including the reported outcomes of treatment in patients with similar mutations. Based on the data available in the literature so far, intensive immunosuppressive treatment is probably not indicated in monogenic nephrotic syndrome if complete or partial remission has not been achieved within 6 weeks of starting treatment. We advocate that family members of individuals with genetic forms of nephrotic syndrome undergo routine genetic testing prior to living-related kidney transplantation. Prospective, multicentre studies are needed to more completely determine the burden of disease caused by monogenic nephrotic syndrome, and randomized controlled trials are needed to clarify the presence or absence of clinical responses of monogenic nephrotic syndrome to available therapies.
MeSH term(s)	Adult ; Child ; Genetic Testing/economics ; Genetic Testing/methods ; Humans ; Insurance Coverage ; Kidney Transplantation ; Nephrotic Syndrome/diagnosis ; Nephrotic Syndrome/genetics ; Nephrotic Syndrome/therapy
Language	English
Publishing date	2013-01-15
Publishing country	England
Document type	Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/nrneph.2012.286
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Zs.A 6334: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 107: Show issues

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Article ; Online: Identification of the SARS-CoV-2 Entry Receptor ACE2 as a Direct Target for Transcriptional Repression by Miz1.

Yang, Jing / Perez, Edith A / Hou, Changchun / Zhang, Pin / Van Scoyk, Michelle / Winn, Robert A / Rong, Lijun / Liu, Jing

Frontiers in immunology

2021 Volume 12, Page(s) 648815

Abstract: Multiple lines of evidence have demonstrated that cigarette smoke or Chronic Obstructive Pulmonary Disease upregulates angiotensin-converting enzyme 2, the cellular receptor for the entry of the severe acute respiratory syndrome coronavirus 2, which ... ...

Abstract	Multiple lines of evidence have demonstrated that cigarette smoke or Chronic Obstructive Pulmonary Disease upregulates angiotensin-converting enzyme 2, the cellular receptor for the entry of the severe acute respiratory syndrome coronavirus 2, which predisposes individuals to develop severe Coronavirus disease 2019. The reason for this observation is unknown. We recently reported that the loss of function of Miz1 in the lung epithelium in mice leads to a spontaneous COPD-like phenotype, associated with upregulation of angiotensin-converting enzyme 2. We also reported that cigarette smoke exposure downregulates Miz1 in lung epithelial cells and in mice, and Miz1 is also downregulated in the lungs of COPD patients. Here, we provide further evidence that Miz1 directly binds to and represses the promoter of angiotensin-converting enzyme 2 in mouse and human lung epithelial cells. Our data provide a potential molecular mechanism for the upregulation of angiotensin-converting enzyme 2 observed in smokers and COPD patients, with implication in severe Coronavirus disease 2019.
MeSH term(s)	Alveolar Epithelial Cells/metabolism ; Angiotensin-Converting Enzyme 2/genetics ; Angiotensin-Converting Enzyme 2/metabolism ; Animals ; BTB-POZ Domain ; Cell Line ; Cigarette Smoking/adverse effects ; Kruppel-Like Transcription Factors/chemistry ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Mice ; Promoter Regions, Genetic ; Protein Binding ; Receptors, Virus/genetics ; Receptors, Virus/metabolism ; SARS-CoV-2/physiology ; Spike Glycoprotein, Coronavirus/metabolism ; Transcription, Genetic/drug effects ; Tumor Necrosis Factors/pharmacology ; Virus Internalization
Chemical Substances	Kruppel-Like Transcription Factors ; Receptors, Virus ; Spike Glycoprotein, Coronavirus ; Tumor Necrosis Factors ; ZBTB17 protein, human ; spike protein, SARS-CoV-2 ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2021-07-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.648815
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Article ; Online: Cooperation between PRMT1 and PRMT6 drives lung cancer health disparities among Black/African American men.

iScience

2024 Volume 27, Issue 2, Page(s) 108858

Abstract: Lung cancer is the third most common cancer with Black/AA men showing higher risk and poorer outcomes than NHW men. Lung cancer disparities are multifactorial, driven by tobacco exposure, inequities in care access, upstream health determinants, and ... ...

Abstract	Lung cancer is the third most common cancer with Black/AA men showing higher risk and poorer outcomes than NHW men. Lung cancer disparities are multifactorial, driven by tobacco exposure, inequities in care access, upstream health determinants, and molecular determinants including biological and genetic factors. Elevated expressions of protein arginine methyltransferases (PRMTs) correlating with poorer prognosis have been observed in many cancers. Most importantly, our study shows that PRMT6 displays higher expression in lung cancer tissues of Black/AA men compared to NHW men. In this study, we investigated the underlying mechanism of PRMT6 and its cooperation with PRMT1 to form a heteromer as a driver of lung cancer. Disrupting PRMT1/PRMT6 heteromer by a competitive peptide reduced proliferation in non-small cell lung cancer cell lines and patient-derived organoids, therefore, giving rise to a more strategic approach in the treatment of Black/AA men with lung cancer and to eliminate cancer health disparities.
Language	English
Publishing date	2024-01-11
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.108858
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Article: Focal and segmental glomerulosclerosis: varying biologic mechanisms underlie a final histopathologic end point.

Daskalakis, Nikki / Winn, Michelle P

Seminars in nephrology

2006 Volume 26, Issue 2, Page(s) 89–94

Abstract: Focal and segmental glomerulosclerosis (FSGS) is a pathologic entity that is a common and increasing cause of end-stage renal disease. Typical manifestations include proteinuria, hypertension, worsening renal insufficiency, and, frequently, renal failure. ...

Abstract	Focal and segmental glomerulosclerosis (FSGS) is a pathologic entity that is a common and increasing cause of end-stage renal disease. Typical manifestations include proteinuria, hypertension, worsening renal insufficiency, and, frequently, renal failure. The etiology, however, remains unknown in a majority of patients. There is an estimated recurrence rate of 30% to 40% in renal transplant patients, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease. Although some of its characteristics have been reported, the precise identification of a circulating factor associated with FSGS has not been made. Remarkable progress has been made in recent years regarding biologic mechanisms surrounding FSGS and proteinuria. Insight into the pathogenesis of FSGS has been gained through the study of hereditary forms of FSGS and nephrotic syndromes. Mutations in cytoskeletal proteins that affect podocyte structure have been the target until recently. Here we review the current understanding of this glomerular disease and areas for future concentration.
MeSH term(s)	Adaptor Proteins, Signal Transducing ; Biomarkers/blood ; Cytoskeletal Proteins/blood ; Disease Progression ; Glomerulosclerosis, Focal Segmental/complications ; Glomerulosclerosis, Focal Segmental/metabolism ; Glomerulosclerosis, Focal Segmental/pathology ; Humans ; Intracellular Signaling Peptides and Proteins ; Kidney Failure, Chronic/etiology ; Kidney Failure, Chronic/pathology ; Membrane Proteins/blood ; Risk Factors ; TRPC Cation Channels/blood ; TRPC6 Cation Channel ; src Homology Domains
Chemical Substances	Adaptor Proteins, Signal Transducing ; Biomarkers ; CD2-associated protein ; Cytoskeletal Proteins ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; NPHS2 protein ; TRPC Cation Channels ; TRPC6 Cation Channel ; TRPC6 protein, human ; nephrin
Language	English
Publishing date	2006-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2005.09.001
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