Camille Macé, PhD

Biography

Camille E. Macé, PhD, is Principal Investigator of the Glomerular Disease Therapeutics Laboratory. During her postdoctoral fellowship, she participated in describing, for the first time, a sialic acid deficient form of the glycoprotein Angiopoietin-like 4 secreted by podocytes in human minimal change nephrotic syndrome as being responsible for the major manifestations of this disease (Nature Medicine 2011). In addition, as a junior faculty, she described the first clear molecular link between proteinuria and hypertriglyceridemia in nephrotic syndrome (Nature Medicine 2014). Furthermore, she is involved in identifying the circulating factors responsible for the pathogenesis of non-HIV collapsing glomerulopathy, with the goal of developing novel therapeutics strategies. Using a combination of animal models and cell culture studies, she was able to establish two experimental mouse models that reproduce the disease and started proteomic analysis of putative circulating factors present in the plasma of recurrent patients. Recently, Macé has been investigating the role of the Zinc Fingers and Homeoboxes 2 transcription factor in the pathogenesis of glomerular disease, and in the viral cytokine storm induced relapse of primary glomerular disease.

Macé received her PhD in France, followed by a postdoctoral fellowship at the University of Alabama at Birmingham. She received a T32 NIH grant and was on faculty at the University of Alabama at Birmingham before joining Rush University. She was funded by an American Heart Association grant. She is presently principal investigator on a NIH R01 grant and co-investigator on an NIH R01 grant.

Publications

Del Nogal Avila M*, Das R*, Kharlyngdoh J*, Molina-Jijon E* (equal contributors), Donoro Blazquez H, Gambut S, Crowley M, Crossman DK, Gbadagesin RA, Chugh SS, Chugh SS, Avila-Casado C, Macé C, Clement LC and Chugh SS. Cytokine storm based mechanisms for extra-pulmonary manifestations of SARS-CoV-2 infection. JCI Insight 2023 (In press). https://insight.jci.org/articles/view/166012

Molina-Jijon E, Gambut S, Macé C, Avila-Casado C, Clement LC. Secretion of the epithelial sodium channel chaperone PCSK9 from the cortical collecting duct links sodium retention with hypercholesterolemia in nephrotic syndrome. Kidney Int. 2020 Dec;98(6):1449-1460. PMID: 32750454

Macé C*, Del Nogal Avila M*, Marshall CB* (equal contributors), Kharlyngdoh J, Das R, Molina-Jijon E, Donoro Blazquez H, Shastry S, Soria E, Wetzels J, Dijkman H, Avila-Casado C, Clement LC and Chugh SS. The zing fingers and homeoboxes 2 protein ZHX2 and its interacting proteins regulate upstream pathways in podocyte diseases. Kidney Int. 2020 Apr;97(4):753-764. PMID: 32059999

Macé C, Clement LC. ManNAc, a new therapeutic agent to reduce Angptl4-induced proteinuria in MCD. Med Sci (Paris). 2016 Jun-Jul;32(6):606-11. PMID: 27406771

Del Nogal-Avila M, Donoro-Blazquez H, Saha MK, Marshall CB, Clement LC, Macé CE, Chugh SS. Novel therapeutic approaches for chronic kidney disease due to glomerular disorders. Am J Physiol Renal Physiol. 2016;311:F63-5. PMID: 27147672

Clement LC, Macé C, Del Nogal Avila M, Marshall CB, Chugh SS. The proteinuriahypertriglyceridemia connection as a basis for novel therapeutics for nephrotic syndrome. Transl Res. 2015 Apr;165(4):499-504. PMID: 25005737

Macé C, Chugh SS. Nephrotic syndrome: components, connections, and angiopoietinlike 4-related therapeutics. J Am Soc Nephrol. 2014 Nov;25(11):2393-8. PMID: 24854282

Macé C, Clément LC. Role of Angptl4 in nephrotic syndrome: a two-faced protein. Med Sci (Paris). 2014 Jun-Jul;30(6-7):605-7. PMID: 25014443

Chugh SS, Macé C, Clement LC, Del Nogal Avila M, Marshall C. Angiopoietin-like 4 based therapeutics for proteinuria and kidney disease. Front Pharmacol. 2014 Feb; 25:5-23. PMID: 24611049

Macé C*, Clement LC* (equal contributors), Avila-Casado C, Kersten S and Chugh SS. Circulating Angiopoietin-like 4 links proteinuria with hypertriglyceridemia in nephrotic syndrome. Nat Med. 2014 Jan; 20: 37–46. PMID: 24317117

Chugh SS, Clement LC, Macé C. New insights into human minimal change disease: Lessons from animal models. Am J Kid Dis. 2012 Feb; 59(2):284-92. Review. PMID: 21974967

Clement LC, Avila-Casado C, Macé C, Soria E, Bakker WW, Kersten S and Chugh SS. Podocyte – secreted Angiopoietin-like-4 mediates proteinuria in glucocorticoidsensitive nephrotic syndrome. Nat Med. 2011 Jan; 17: 117-122. PMID: 21151138

Tré-Hardy M, Macé C, El Manssouri N, Vanderbist F, Traore H, and Devleeschouwer MJ. Effect of antibiotic co-administration on young and mature biofilms of cystic fibrosis clinical isolates; the importance of the biofilm model. Int J Antimicrob Agents. 2009 Jan; 33:40–45. PMID: 18801647

Macé C, Seyer D, Chemani C, Cosette P, Di-Martino P, Guery B, Filloux A, Fontaine M, Molle V, Junter GA and Jouenne T. Identification of biofilm-associated cluster (bac) in Pseudomonas aeruginosa involved in biofilm formation and virulence. PLoS ONE.2008;3(12):e3897. PMID: 19065261

Grants

1)NIH 1R01DK133330 (March 15 2023 to December 31 2027)
Principal Investigator Camille Macé
Co-Investigator Lionel C. Clement
Title: COVID-19-induced worsening of glomerular diseases
Brief summary: This proposal will study the effect of cytokine storm, released during COVID-19 infection, in worsening preexisting glomerular disease in animal models of focal segmental glomerulosclerosis and diabetic nephropathy, with the goal of developing novel therapeutic strategy.

2) NIH 1R01DK128203 (May 1 2021 to April 30 2026)
Principal Investigator Sumant S. Chugh
Co-Investigator Camille Macé
Title: Soluble mediators of relapse
Brief summary: This proposal will investigate the cytokine storm induced by common cold infections to prevent relapse of minimal change disease and focal and segmental glomerulosclerosis.

3) NIH 1R01DK111102 (September 1 2016 to August 31 2021)
Principal Investigator Sumant S. Chugh
Co-Investigator Camille Macé
Title: Investigation of non-HIV collapsing glomerulopathy
Brief summary: This study indentifies nephritogenic circulating proteins that cause reccurent non-HIV collapsing glomerulopathy, and explores molecular mechanisms of podocyte proliferation, capillary loop collapse and in vivo crosstalk.

4) AHA Scientist Development Grant 16SDG27500017 (January 2016 to December 2019)
Mentor: Sumant S. Chugh
Principal Investigator: Camille Macé
Title: Molecular mechanisms of non-HIV collapsing glomerulopathy
This proposal will conduct in vitro studies on mechanisms involved in collapsing glomerulopathy

5) NIH T32DK007545 (July 1 2012 to June 30214)
Ruth L. Kirschstein National Research Service Award (NRSA)
Principal Investigator: Camille Macé
Title: Investigation of non-HIV collapsing glomerulopathy

Education

Research Areas