Bellusci lab

2017_El Agha CSC 2017 from Saverio Bellusci, Ph D on Vimeo.

 

2017_El Agha_Cell Stem Cell.

We have used genetic engineering in mice to identify precursor cells for activated myofibroblasts and investigate their fate in a reversible model of lung fibrosis. Our findings emphasize the phenotypic plasticity of lipogenic and myogenic lung fibroblasts and indicate that PPARg  agonists might be beneficial in treating IPF.

2017_Moisenko_StemCells_v3 from Saverio Bellusci, Ph D on Vimeo.

  

2017_Moiseenko_Stem cells

The developmental origin of the smooth muscle cells in the lung is still controversial. We used a lineage-tracing based approach combined with immunofluorescence, FACS and gene arrays to quantify the respective contribution of different mesenchymal progenitors to the SMC lineage. We also compared, at E18.5, the transcriptomic profile of alveolar myofibroblast progenitors versus bone fide ACTA2+ cells (vascular and airway SMC).

2015_Al Alam et final from Saverio Bellusci, Ph D on Vimeo.

  

2015_Al Alam et al_Development

Although lipofibroblasts were initially believed merely to assist type 2 alveolar epithelial cells in surfactant production during neonatal life, recent evidence suggests that these cells are indispensable for survival and growth of epithelial stem cells during adulthood. We show that a population of lipid-droplet-containing stromal cells emerges in the developing mouse lung between E15.5 and E16.5. This is accompanied by significant upregulation, in the lung mesenchyme, of peroxisome proliferator-activated receptor gamma (master switch of lipogenesis), adipose differentiation-related protein (marker of mature lipofibroblasts) and fibroblast growth factor 10 (previously shown to identify a subpopulation of lipofibroblast progenitors). Using genetically modified mice to interfere with Fgf10 signaling, we demonstrate  an essential role for Fgf10 signaling in the formation of lipofibroblasts during late lung development.

miR142 from Saverio Bellusci, Ph D on Vimeo.

 

We found that microRNA142-3p is expressed at high level in the embryonic lung mesenchyme. This paper reports the role in vitro of miR142 during early lung development using a knockdown approach. We demonstrate that Adenomatous Polyposis Coli  (Apc) is the major target of miR142. Accordingly to Apc's role in canonical Wnt signaling, miR142 knockdown-associated Apc up-regulation leads to inhibition of Wnt signaling. Such inhibition leads to arrested proliferation and premature differentiation of airway smooth muscle cells progenitors. We also show that the effect of miR142 knock down can be rescued by the deletion of one copy of Apc or by induced expression of an activated for of beta-catenin in the lung mesenchyme. The validation of these results in vivo is currently underway.

Saverio Bellusci interviews Clarence Wigfall from Saverio Bellusci, Ph D on Vimeo.

 

Saverio Bellusci interviews former student, Clarence Wigfall, about his impressions of joining the Bellusci Lab in Los Ageles, California and spending 4 years working and studying there.

Wigfall won a 2014 Federation of American Societies For Experimental Biology (FASEB) BioArt Award for his work in creating the video - Distal Lung Airway - from microCT scans, resolution +/- 5 microns.

Wigfall is, as of, November 2014, completing an MPH and doing an Applied Social Psychology PhD at Claremont Graduate University in Southern California

2014 Gordon Conference - Fibroblast Growth Factors in Development & Disease Re-Cap

Held March 2-7, 2014   Ventura, CA

Clarence Wigfall, of Advanced Science Communications, interview with Dr. Bellusci Re-Capping the 2014 Gordon Conference on Fibroblast Growth Factors.

GRC ReCap by Saverio Bellusci, PhD from Saverio Bellusci, Ph D on Vimeo.

 

The Gordon Research Seminar on Fibroblast Growth Factors in Development & Disease is a unique forum for graduate students, post-docs, and other scientists with comparable levels of experience and education to present and exchange new data and cutting edge ideas.

The focus of this meeting was emerging research on molecular mechanisms of FGF signaling and the involvement of these pathways in normal development and pathological conditions as well as in regeneration/repair after injury. The meeting covered diverse areas of FGF biology including, but not limited to, developmental biology, cell biology, pathology, pharmacology, endocrinology and biochemistry.