Cellular Network In Generation and Degeneration

Fabio Rossi, M.D., Ph.D.
Professor, Department of Medical Genetics
Professor, School of Biomedical Engineering
Director, Biomedical Research Centre
Director of Research, School of Biomedical Engineering
Founder of the BC Regenerative Medicine Cluster

Rossi Lab Website
Lab Members


Three scientific directions:

Three distinct but interrelated research directions are active in the laboratory:

Cellular systems in muscle regeneration
Adult muscle usually regenerates very efficiently. However when regeneration fails, for example due to repeated damage or alterations in the inflammatory milieu, deposition of fibrotic matrix infiltrated with adipocytes takes place and initiates a vicious circle that prevents functional restoration and interferes with therapeutic approaches. We identified and isolated the progenitors responsible for such “fibrofatty infiltration”. These perivascular mesenchymal cells were initially called fibro-adipogenic progenitors (FAPs) due to their prevalent developmental potential, but recent work from the Goldhamer lab has clearly shown that the same cells are the origin of the ectopic ossification often observed after extensive muscle damage and that they can be induced to acquire an osteogenic phenotype by exposure to BMP2 in vitro. Thus, we now believe these cells to represent the in vivo counterparts of mesenchymal stem cells (MSCs).

From the point of view of progenitor activity, the response of skeletal muscle to damage can be divided in two main phases:

Expansion phase (first 3-4 days following damage) Muscle resident MSCs respond to acute damage by entering a proliferative phase that coincides with the expansion of myogenic progenitors (satellite cells). During this phase, activated MSCs provide trophic support from myogenic cells, and the molecules involved in this crosstalk are the objects of intense investigation in the lab. Throughout this phase inflammatory macrophages reach the tissue through the bloodstream (also called M1 type) and represent the predominant type of inflammatory cells.

Extinction phase (from day 4 to day 7 after damage) As satellite cells abruptly cease to proliferate, they differentiate, fuse to damaged myofibers and return to pre-damage numbers. When regeneration is efficient, a similar fate is met by MSCs. During this phase, M1 macrophages rapidly decrease and are replaced by M2-type, pro-regenerative macrophages. However, if regeneration is inefficient, these cells are retained in the tissue and differentiate in fibrogenic cells as well as adipocytes, initiating fibrofatty degeneration. Another focus of our work is the identification of the cellular and molecular mechanisms underlying their disappearance, and how they fail during the establishment of fibrosis.

Role of innate immune cells Marcophages are required for proper regeneration, which can be disrupted by blocking either the M1-M2 transition, or by preventing the first wave of circulating monocytes from reaching the tissue from the circulation. In both cases, the result is the deposition of fibrotic matrix and the appearance of adipocytes. The interplay between satellite cells, monocytes and MSCs is a key interest of the laboratory.

Microglia/macrophages in CNS pathology
Micorglia are essentially indistinguishable from mature tissue macrophages, but have different functional properties. The investigation of the relative role of these inflammatory cell subsets in CNS pathology has been hindered by the fact that the method routinely used for the generation of chimeric mice requires myeloablation by irradiation, which affects the blood-brain barrier, and the forced mobilization and injection in the bloodstream of hematopoietic progenitors that would normally not exit the bone marrow environment. This leads to the artifactual replacement of microglial cells with bone marrow derived cells. We use an alternative method method to generate chimeras which is alternative method to generate chimeras which is based on parabiosis (the surgical joining of two immunocompatible adult mice leading to blood sharing) we were able to show that microglia is capable of self renewing within the CNS and it is not dependent on bone marrow resident hematopoietic stem cells. This finding was later confirmed by others, which showed that microglia originates from yolk sac hematopoiesis early during development, and not from bone marrow hematopoietic stem cells. Taking advantage of this unique system, we have recently shown that blood derived cells infiltrating the CNS cause the progression of EAE, a mouse model of Multiple Sclerosis to paralysis stages. In addition, we also realized that even when bone marrow derived cells enter the CNS they are unable to replace the endogenous microglia, and they eventually disappear

Ongoing work in the lab addresses questions such as:

What molecular differences allow microglia but not bone marrow derived macrophages to self renew in the CNS? What determines whether innate immune cells cross (e.g. in MS) or not (e.g. following axotomy or in ALS) the blood brain barrier? How do microglia and bone marrow derived myelomonocytic cells change from induction to remission of EAE?

Epigenetic control of lineage choice/differentiation
The last decade of work and the recent Nobel prize awarded for reprogramming has made it clear that cell identity is established and maintained by combinations of transcription factors. A role for epigenetic regulators such as histone methyltransferases in establishing and maintaining cell fate has been hypothesized, but investigations of the role of these enzymes in complex biological systems have lagged behind their biochemical characterization. To bridge such gap, we have generated floxed alleles of two SET-domain (methyltransferase) containing genes encoding for putative methytransferases. Based on in vitro experiments SET7/9 had been described as a H3K4 monomethyltransferase (now questioned) capable of methylating a number of important transcription factors including p53 and the estrogen receptor. Despite reports that SET7 activity is a requirement for these transcription factors to function, KO mice for SET7/9 were viable, fertile and did not display any defect in p53 pathways. As these data was controversial and anti-dogmatic, it took over three years of a rather byzantine review process for this work to be published. This should function as a cautionary tale on the dangers of basing strong biological conclusions on in vitro data, and as a message to reviewers and editors that resistance is futile, and that eventually the truth will prevail and they will publish our papers! Further investigations in the role of SET7/9 are ongoing in collaboration with the Zaph laboratory.

EHMT2/G9a is a H3K9 dimethyltransferase, although it has been suggested that it may also methylate other residues on histone tails. Complete KO of this enzyme was shown to lead to early lethality, prompting us to generate a floxed allele to analyze its roles in adult organisms.
In particular, we have focused on the analysis of its role in hematopoiesis. To our surprise, G9a deletion did not lead to an overt phenotype, and although alterations in T-cell polarization were characterized and reported by our next-door collaborator Colby Zaph, no defect in stem cells activity was observed when using sensitive competitive transplantation assays.
The first hint of a G9a dependent phenotype in immature hematopoietic cells stemmed from the observation that the colonies formed by G9a KO bone marrow derived progenitors when plated in methylcellulose were significantly smaller than those obtained from control heterozygous animals. This led us to test the role of G9a in leukemia, and eventually to the finding that G9a is required for aggressive acute myeloid leukemia, and that in its absence leukemic cells differentiate at a high rate.

Selected Publications

Microglia’s heretical self-renewal
Fabio Rossi and Coral lewis
Nature Neuroscience news & views, March 2018

Inhibition of Methyltransferase Setd7 Allows the in Vitro Expansion of Myogenic Stem Cells with Improved Therapeutic Potential.
Robert N. Judson, Marco Quarta Menno J. Oudhoff Hesham Soliman Lin Yi Chih Kai Chang Gloria Loi Ryan Vander Werff Alissa Cait Mark HamerJustin Blonigan Patrick Paine Linda T.N. Doan Elena Groppa WenJun He Le Su Regan H. Zhang
Peter Xu Christine Eisner Marcela Low Ingrid Barta Coral-Ann B. Lewis Colby Zaph Mohammad M. Karimi
Thomas A. Rando Fabio M. Rossi
Cell Stem Cel, January 23rd, 2018l: http://www.cell.com/cell-stem-cell/fulltext/S1934-5909(17)30511-8

Increased non-HDL cholesterol levels cause muscle wasting and ambulatory dysfunction in the mouse model of LGMD2B.
Sellers SL, Milad N, White Z, Pascoe CD, Chan R, Payne GW, Seow CY, Rossi F, Seidman MA, Bernatchez P.
J Lipid Res. 2017 Nov 25. pii: jlr.M079459. doi: 10.1194/jlr.M079459. [Epub ahead of print]

Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophy.
Milad N, White Z, Tehrani AY, Sellers S, Rossi FMV, Bernatchez P.
Skelet Muscle. 2017 Sep 12
PMID: 28899419

Isolation, Culture, and Differentiation of Fibro/Adipogenic Progenitors (FAPs) from Skeletal Muscle.
Judson RN, Low M, Eisner C, Rossi FM.
Methods Mol Biol. 2017;1668:93-103
PMID: 28842904

A blueprint for the next generation of ELSI research, training, and outreach in regenerative medicine.
Illes J, Sipp D, Kleiderman E, Benjaminy S, Isasi R, Lomax G, Master Z, McCormick J, Ogbogu U, Ravitsky V, Robillard JM, Rossi F, Wilson B, Zarzeczny A.
NPJ Regen Med. 2017 Jul 5;2:21. doi: 10.1038/s41536-017-0026-z. eCollection 2017. Review.

Loss of Vascular CD34 Results in Increased Sensitivity to Lung Injury.
Lo BC, Gold MJ, Scheer S, Hughes MR, Cait J, Debruin E, Chu FSF, Walker DC, Soliman H, Rossi FM, Blanchet MR, Perona-Wright G, Zaph C, McNagny KM.
Am J Respir Cell Mol Biol. 2017 Jul 6. doi: 10.1165
PMID: 28683207

Bone Marrow-Derived Cell Accumulation in the Spinal Cord Is Independent of Peripheral Mobilization in a Mouse Model of Amyotrophic Lateral Sclerosis.
Peake K, Manning J, Lewis CA, Tran K, Rossi F, Krieger C.
Front Neurol. 2017 Mar 8;8:75.
PMID: 28337172

Fibro/Adipogenic Progenitors (FAPs): Isolation by FACS and Culture.
Low M, Eisner C, Rossi F.
Methods Mol Biol. 2017;1556:179-189
PMID: 28247350

Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration.Pisconti A, Banks GB, Babaeijandaghi F, Betta ND, Rossi FM, Chamberlain JS, Olwin BB.
Skelet Muscle. 2016 Oct 4;6:34.
PMID: 27757223

Pharmacological blockage of fibro/adipogenic progenitor expansion and suppression of regenerative fibrogenesis is associated with impaired skeletal muscle regeneration.
Fiore D, Judson RN, Low M, Lee S, Zhang E, Hopkins C, Xu P, Lenzi A, Rossi FM, Lemos DR.
Stem Cell Res. 2016 Jul;17(1):161-9. doi: 10.1016/j.scr.2016.06.007.
PMID: 27376715

G9a regulates group 2 innate lymphoid cell development by repressing the group 3 innate lymphoid cell program.
Antignano F, Braam M, Hughes MR, Chenery AL, Burrows K, Gold MJ, Oudhoff MJ, Rattray D, Halim TY, Cait A, Takei F, Rossi FM, McNagny KM, Zaph C.
J Exp Med. 2016 Jun 27;213(7):1153-62. doi: 10.1084/jem.20151646.
PMID: 27298444

The lysine methyltransferase Ehmt2/G9a is dispensable for skeletal muscle development and regeneration.
Zhang RH, Judson RN, Liu DY, Kast J, Rossi FM.
Skelet Muscle. 2016 May 27;6:22. doi: 10.1186/s13395-016-0093-7. eCollection 2016.

SETD7 Controls Intestinal Regeneration and Tumorigenesis by Regulating Wnt/β-Catenin and Hippo/YAP Signaling. Oudhoff MJ, Braam MJ, Freeman SA, Wong D, Rattray DG, Wang J, Antignano F, Snyder K, Refaeli I, Hughes MR, McNagny KM, Gold MR, Arrowsmith CH, Sato T, Rossi FM, Tatlock JH, Owen DR, Brown PJ, Zaph C. 2016 Dev Cell 37(1):47-57

Origin, fate and dynamics of macrophages at CNS interface.
Tobias Goldmann, Peter Wieghofer, Marta Joana Costa Jordão,
Fabiola Prutek, Nora Hagemeyer, Kathrin Frenzel, Lukas Amann,
Ori Staszewski, Katrin Kierdorf, Martin Krueger, Giuseppe Locatelli, Hannah Hochgarner, Robert Zeiser, Slava Epelman, Frederic Geissmann,
Josef Priller, Fabio Rossi, Ingo Bechmann, Martin Kerschensteiner,
Sten Linnarsson, Steffen Jung, Marco Prinz.
Nature Immunology. 2016, doi: 10.1038/ni.3423 PMID:27135602

Perhexiline maleate enhances antitumor efficacy of cisplatin in neuroblastoma by inducing over-expression of NDM29 ncRNA.
Vella S, Penna I, Longo L, Pioggia G, Garbati P, Florio T, Rossi F, Pagano A
Sci Rep. 2015 Dec 17;5:18144. doi: 10.1038/srep18144.

Skeletal muscle-resident MSCs and bone formation.
Lemos DR, Eisner C, Hopkins CI, Rossi FM.
Bone. 2015 Jun 21. pii: S8756-3282(15)00249-5. doi: 10.1016/j.bone.2015.06.013. [Epub ahead of print] Review.
PMID: 26103092

Nilotinib reduces muscle fibrosis in chronic muscle injury by promoting TNF-mediated apoptosis of fibro/adipogenic progenitors.
Dario R Lemos, Farshad Babaeijandaghi, Marcela Low, Chih-Kai Chang, Sunny T Lee, Daniela Fiore, Regan-Heng Zhang, Anuradha Natarajan, Sergei A Nedospasov & Fabio M V Rossi.
Nat Med. 2015 Jul;21(7):786-94.
PMID: 26053624

Busulfan as a myelosuppressive agent for generating stable high-level bone marrow chimerism in mice.
Peake K, Manning J, Lewis CA, Barr C, Rossi F, Krieger C.
J Vis Exp. 2015 Apr 1;(98)
PMID: 25867947

Submyeloablative conditioning with busulfan permits bone marrow-derived cell accumulation in a murine model of Alzheimer’s disease.
​Barr CM, Manning J, Lewis CA, Rossi FM, Krieger C.
Neurosci Lett. 2015 Feb 19;588:196-201
PMID: 25582787

Inflammation in muscle repair, aging, and myopathies.
Bouché M, Muñoz-Cánoves P, Rossi F, Coletti D.
Biomed Res Int. 2014;2014:821950. doi: 10.1155/2014/821950. Epub 2014 Aug 4. No abstract available.
PMID: 25162030 [PubMed – in process] Free Article

The role of microglia in human disease: therapeutic tool or target?
Cartier N, Lewis CA, Zhang R, Rossi FM.
Acta Neuropathol. 2014 Sep;128(3):363-80. doi: 10.1007/s00401-014-1330-y. Epub 2014 Aug 9.
PMID: 25107477 [PubMed – in process] Free PMC Article

(R)-PFI-2 is a potent and selective inhibitor of SETD7 methyltransferase activity in cells.
Barsyte-Lovejoy D, Li F, Oudhoff MJ, Tatlock JH, Dong A, Zeng H, Wu H, Freeman SA, Schapira M, Senisterra GA, Kuznetsova E, Marcellus R, Allali-Hassani A, Kennedy S, Lambert JP, Couzens AL, Aman A, Gingras AC, Al-Awar R, Fish PV, Gerstenberger BS, Roberts L, Benn CL, Grimley RL, Braam MJ, Rossi FM, Sudol M, Brown PJ, Bunnage ME, Owen DR, Zaph C, Vedadi M, Arrowsmith CH.
Proc Natl Acad Sci U S A. 2014 Aug 18. pii: 201407358. [Epub ahead of print]
PMID: 25136132 [PubMed – as supplied by publisher]

Collision or convergence?: Beliefs and politics in neuroscience discovery, ethics, and intervention.
Paylor B, Longstaff H, Rossi F, Illes J.
Trends Neurosci. 2014 Aug;37(8):409-12. doi: 10.1016/j.tins.2014.06.001.
PMID: 25086860 [PubMed – in process]

In vivo characterization of neural crest-derived fibro/adipogenic progenitor cells as a likely cellular substrate for craniofacial fibrofatty infiltrating disorders.
Paylor B, Joe AW, Rossi FM, Lemos DR.
Biochem Biophys Res Commun. 2014 Aug 15;451(1):148-51. doi: 10.1016/j.bbrc.2014.07.089. Epub 2014 Jul 26.
PMID: 25073114 [PubMed – in process]

Methyltransferase G9A regulates T cell differentiation during murine intestinal inflammation.
Antignano F, Burrows K, Hughes MR, Han JM, Kron KJ, Penrod NM, Oudhoff MJ, Wang SK, Min PH, Gold MJ, Chenery AL, Braam MJ, Fung TC, Rossi FM, McNagny KM, Arrowsmith CH, Lupien M, Levings MK, Zaph C.
J Clin Invest. 2014 May 1;124(5):1945-55. doi: 10.1172/JCI69592. Epub 2014 Mar 25.
PMID: 24667637 [PubMed – indexed for MEDLINE] Free PMC Article

The methyltransferase G9a regulates HoxA9-dependent transcription in AML.
Lehnertz B, Pabst C, Su L, Miller M, Liu F, Yi L, Zhang R, Krosl J, Yung E, Kirschner J, Rosten P, Underhill TM, Jin J, Hébert J, Sauvageau G, Humphries RK, Rossi FM.
Genes Dev. 2014 Feb 15;28(4):317-27. doi: 10.1101/gad.236794.113.
PMID: 24532712 [PubMed – in process]
Related citations

Tissue-resident mesenchymal stem/progenitor cells in skeletal muscle: collaborators or saboteurs?
Judson RN, Zhang RH, Rossi FM.
FEBS J. 2013 Sep;280(17):4100-8. doi: 10.1111/febs.12370. Epub 2013 Jun 24. Review.
PMID:23763717[PubMed – indexed for MEDLINE] Related citations

Control of the hippo pathway by Set7-dependent methylation of Yap.
Oudhoff MJ, Freeman SA, Couzens AL, Antignano F, Kuznetsova E, Min PH, Northrop JP, Lehnertz B, Barsyte-Lovejoy D, Vedadi M, Arrowsmith CH, Nishina H, Gold MR, Rossi FM, Gingras AC, Zaph C.
Dev Cell. 2013 Jul 29;26(2):188-94. doi: 10.1016/j.devcel.2013.05.025. Epub 2013 Jul 11.
PMID:23850191[PubMed – indexed for MEDLINE] Related citations

Tissue-resident Sca1+ PDGFRα+ mesenchymal progenitors are the cellular source of fibrofatty infiltration in arrhythmogenic cardiomyopathy.
Paylor B, Fernandes J, McManus B, Rossi F.
F1000Res. 2013 Jun 19;2. doi: 10.12688/f1000research.2-141.v1.
PMID: 24358871[PubMed – as supplied by publisher]

Myelosuppressive conditioning using busulfan enables bone marrow cell accumulation in the spinal cord of a mouse model of amyotrophic lateral sclerosis.
Lewis CA, Manning J, Barr C, Peake K, Humphries RK, Rossi F, Krieger C.
PLoS One. 2013 Apr 8;8(4):e60661. doi: 10.1371/journal.pone.0060661. Print 2013.
PMID:23593276[PubMed – indexed for MEDLINE] Free PMC ArticleRelated citations

Role of Stem/Progenitor Cells in Reparative Disorders.
Pretheeban T, Lemos DR, Paylor B, Zhang RH, Rossi FM.
Fibrogenesis Tissue Repair. 2012 Dec 27;5(1):20. doi: 10.1186/1755-1536-5-20.
PMID:23270300[PubMed] Free PMC ArticleRelated citations

In vivo evaluation of calcium polyphosphate for nine regeneration.
Comeau PA, Frei H, Yang C, Fernlund G, Rossi FM.
J Biomater Appl. 2012 Sep 27(3):267-75. doi: 10.1177/0885328211401933. Epub 2011 Sep 16.

The Neuroinflammatory Response in ALS: The Roles of Microglia and T Cells.
Lewis CA, Manning J, Rossi F, Krieger C.
Neurol Res Int. 2012;2012:803701. doi: 10.1155/2012/803701. Epub 2012 May 15.
PMID:22666587[PubMed] Free PMC ArticleRelated citations

Functionally Convergent White Adipogenic Progenitors of Different Lineages Participate in a Diffused System Supporting Tissue Regeneration.
Lemos DR, Paylor B, Chang C, Sampaio A, Underhill TM, Rossi FM.
Stem Cells. 2012 Mar 13. doi: 10.1002/stem.1082. [Epub ahead of print]
PMID: 22415977 [PubMed – as supplied by publisher]

Deconstruction of the SS18-SSX fusion oncoprotein complex: insights into disease etiology and therapeutics.
Su L, Sampaio AV, Jones KB, Pacheco M, Goytain A, Lin S, Poulin N, Yi L, Rossi FM, Kast J, Capecchi MR, Underhill TM, Nielsen TO.
Cancer Cell. 2012 Mar 20;21(3):333-47. doi: 10.1016/j.ccr.2012.01.010.
PMID:22439931[PubMed – indexed for MEDLINE] Free PMC ArticleRelated citations

Targeted cell fusion facilitates stable heterokaryon generation in vitro and in vivo.
Long MA, Rossi FM.
PLoS One. 2011;6(10):e26381. Epub 2011 Oct 24.

CD34 Promotes Satellite Cell Motility and Entry into Proliferation to Facilitate Efficient Skeletal Muscle Regeneration.
Alfaro LA, Dick SA, Siegel AL, Anonuevo AS, McNagny KM, Megeney LA, Cornelison DD, Rossi FM.
Stem Cells. 2011 Dec;29(12):2030-41. doi: 10.1002/stem.759.

p53-dependent transcription and tumor suppression are not affected in Set7/9-deficient mice.
Lehnertz B, Rogalski JC, Schulze FM, Yi L, Lin S, Kast J, Rossi FM.
Mol Cell. 2011 Aug 19;43(4):673-80.

Prolonged self-renewal activity unmasks telomerase control of telomere homeostasis and function of mouse hematopoietic stem cells.
Sekulovic S, Gylfadottir V, Vulto I, Gasparetto M, Even Y, Brookes C, Smith C, Eaves CJ, Lansdorp PM, Rossi FM, Humphries RK.
Blood. 2011 Aug 18;118(7):1766-73. Epub 2011 Jul 5.

Infiltrating monocytes trigger EAE progression, but do not contribute to the resident microglia pool.
Ajami B, Bennett JL, Krieger C, McNagny KM, Rossi FM.
Nat Neurosci. 2011 Jul 31;14(9):1142-9. doi: 10.1038/nn.2887.

Lysine methyltransferase G9a is required for de novo DNA methylation and the establishment, but not the maintenance, of proviral silencing.
Leung DC, Dong KB, Maksakova IA, Goyal P, Appanah R, Lee S, Tachibana M, Shinkai Y, Lehnertz B, Mager DL, Rossi F, Lorincz MC.
Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5718-23. Epub 2011 Mar 22.

Purification of progenitors from skeletal muscle.
Yi L, Rossi F.
J Vis Exp. 2011 Mar 16;(49). pii: 2476. doi: 10.3791/2476.

Fibro/adipogenic progenitors: a double-edged sword in skeletal muscle regeneration.
Natarajan A, Lemos DR, Rossi FM.
Cell Cycle. 2010 Jun 1;9(11):2045-6. Epub 2010 Jun 1. No abstract available.

Muscle injury activates resident fibro/adipogenic progenitors that facilitate myogenesis.
Joe AW, Yi L, Natarajan A, Le Grand F, So L, Wang J, Rudnicki MA, Rossi FM.
Nat Cell Biol. 2010 Feb;12(2):153-63. Epub 2010 Jan 17.

Activating and inhibitory functions for the histone lysine methyltransferase G9a in T helper cell differentiation and function.
Lehnertz B, Northrop JP, Antignano F, Burrows K, Hadidi S, Mullaly SC, Rossi FM, Zaph C.
J Exp Med. 2010 May 10;207(5):915-22. Epub 2010 Apr 26.

CD34 mediates intestinal inflammation in Salmonella-infected mice.
Grassl GA, Faustmann M, Gill N, Zbytnuik L, Merkens H, So L, Rossi FM, McNagny KM, Finlay BB.
Cell Microbiol. 2010 Nov;12(11):1562-75. doi: 10.1111/j.1462-5822.2010.01488.x.

Effects of granulocyte-colony stimulating factor on bone marrow-derived progenitor cells in murine cardiac transplantation.
Rezai N, Deisher TA, Heine HL, Wang X, Corbel SY, Leung J, Kerjner A, Rossi FM, Podor TJ, McManus BM.
Cardiovasc Pathol. 2010 Jan-Feb;19(1):36-47. Epub 2009 Jan 14. No abstract available.

Thymic progenitor homing and lymphocyte homeostasis are linked via S1P-controlled expression of thymic P-selectin/CCL25.
Gossens K, Naus S, Corbel SY, Lin S, Rossi FM, Kast J, Ziltener HJ.
J Exp Med. 2009 Apr 13;206(4):761-78. Epub 2009 Mar 16.

Depot-specific differences in adipogenic progenitor abundance and proliferative response to high-fat diet.
Joe AW, Yi L, Even Y, Vogl AW, Rossi FM.
Stem Cells. 2009 Oct;27(10):2563-70.

Bone marrow-derived cells in the central nervous system of a mouse model of amyotrophic lateral sclerosis are associated with blood vessels and express CX(3)CR1.
Lewis CA, Solomon JN, Rossi FM, Krieger C.
Glia. 2009 Oct;57(13):1410-9.

The differential in vitro and in vivo responses of bone marrow stromal cells on novel porous gelatin-alginate scaffolds.
Yang C, Frei H, Rossi FM, Burt HM.
J Tissue Eng Regen Med. 2009 Dec;3(8):601-14

Silencing inhibits Cre-mediated recombination of the Z/AP and Z/EG reporters in adult cells.
Long MA, Rossi FM.
PLoS One. 2009;4(5):e5435. Epub 2009 May 5.

Extensive fusion of haematopoietic cells with Purkinje neurons in response to chronic inflammation.
Johansson CB, Youssef S, Koleckar K, Holbrook C, Doyonnas R, Corbel SY, Steinman L, Rossi FM, Blau HM.
Nat Cell Biol. 2008 May;10(5):575-83. Epub 2008 Apr 20.

Local self-renewal can sustain CNS microglia maintenance and function throughout adult life.
Ajami B, Bennett JL, Krieger C, Tetzlaff W, Rossi FM.
Nat Neurosci. 2007 Dec;10(12):1538-43. Epub 2007 Nov 18.


Farshad Babaeijandaghi,PhD Student
Vittoria Canale, Research and Executive Assistant
Chikai Chang, Research Assistant/Technician
Christine Eisner, PhD Student
Elena Groppa, Postdoctoral Fellow
Mark Hammer, CYTOF Manager
Nasim Kajabadi, PhD Student
Marine Theret, Postdoctoral Fellow
Lin Yi, Research Assistant/Technician