Ricardo Battaglino, PhD
Assistant Member of the Staff
Department of Cytokine Biology
email: rbattaglino at forsyth.org
University of Buenos Aires, School of Sciences, MSc, 1985, Biochemistry/Molecular Biology
Mount Sinai, Graduate School, PhD, 1997, Developmental Molecular Biology
Dr. Battaglino's research focuses on the biology of Osteoclast Differentiation and Activation. Osteoclasts are multinucleated cells of the monocyte-macrophage lineage that form by fusion of mononuclear precursors. This multistep differentiation process is under the control of the bone microenvironment that includes stromal cells, osteoblasts, and local factors. Bone resorption by osteoclasts (OC) is required for normal modeling and remodeling of bone. Excessive resorption is an important pathologic feature of many diseases, including osteoporosis, arthritis, periodontitis, and the hypercalcemia of malignancy. Although several key regulators of osteoclast formation and activation have recently been characterized, many gaps in our knowledge still remain.
Using differential cDNA screening and gene array approaches Dr. Battaglino has isolated and characterized a number of novel genes that are predominantly expressed in osteoclasts. As information from the human and mouse genome projects accrues, Dr. Battaglino seeks to define the complete array of osteoclast genes using these approaches.
Of great interest, Dr. Battaglino has recently described a role for serotonin in osteoclast development. Skeletal-Neural Interactions are an exciting new arena of bone research involving neuromodulation of bone cells by neuropeptides and neurotransmitters.
Serotonin (5HT) is a neurotransmitter that controls many vital body functions affecting mood, anxiety, depression, arousal, impulses, and aggression. The extracellular and intracellular levels of serotonin are controlled by a transporter (5-HTT) that regulates the uptake and availability of this mediator. Dr. Battaglino recently found that this serotonin transporter is involved in osteoclast differentiation. He has also recently found that the popular antidepressant Fluoxetine (Prozac) signals through this serotonin transporter in osteoclasts to blocks this activity and increase bone mass in mice. These findings have exciting implications for osteoporosis treatment in humans. His future work in this area will focus on the precise mechanisms involved in serotonin signaling in bone cells.
Dr. Battaglino has also recently described a novel gene involved in osteoclast development, which he calls the NHE-oc. This gene regulates a previously undescribed mechanism to control osteoclast numbers and ultimately the rate of bone remodeling. He is currently studying a possible role for NHE-oc in mitochondrial mediated osteoclast apoptosis. Finally, in conjunction with researchers in the Department of Physical Medicine and Rehabilitation, Harvard Medical School, Dr. Battaglino is working to understand the severe bone loss that occurs following neurological injury, including spinal cord injury. This work has very exciting translational and clinical implications since there is no current treatment for osteoporosis in SCI patients.
Morse LR, Lazzari AA, Battaglino R, Stolzmann KL, Matthess KR, Gagnon DR, Davis SA, Garshick E. 2009. Dual energy x-ray absorptiometry of the distal femur may be more reliable than the proximal tibia in spinal cord injury. Arch Phys Med Rehabil. 90(5):827-31.
Battaglino RA, Vokes M, Späte U, Sharma A, Graves D, Kohler T, Muller R, Yoganathan S, Stashenko P. 2007. Fluoxetine treatment increases trabecular bone formation in mice. J. Cell. Biochem. 100(6): 1387-1394.
Schulze-Späte U, Battaglino R, Fu J, Sharma A, Vokes M, Stashenko P. 2007. Brn3 Transcription factors control terminal osteoclastogenesis J. Cell Biochem. 102(1): 1-12. Pham L, Purcell P, Morse LR, Stashenko P, Battaglino RA. 2007. Expression Analysis of nha-oc/NHA2: A novel osteoclast-specific gene. Gene Expr. Patterns 7(8): 846-851.
Gyurko R, Shoji H, Battaglino RA, Boustany G, Gibson FC III, Genco CA, Stashenko P, Van Dyke TE. 2005. Inducible nitric oxide synthase mediates bone development and P. gingivalisinduced alveolar bone loss. Bone 36(3) :472–479.
Battaglino R, Fu J, Späte U, Ersoy U, Joe M, Sedaghat L, Stashenko P. 2004. Serotonin regulates osteoclasts differentiation through its transporter. J. Bone Miner. Res. 19(9):1420–1431.
Okamatsu Y, Kim D, Battaglino R, Sasaki H, Späte U, Stashenko P. 2004. MIP-1g promotes receptor activator of NF-kB ligand-induced osteoclast formation and survival. J. Immunol. 173(3):2084–2090.
Battaglino R, Kim D, Fu J, Vaage B, Fu XY, Stashenko P. 2002. c-myc is required for osteoclast differentiation. J. Bone Miner. Res. 17(5):763–773.
Xiong J, Battaglino R, Stuhlmann H. 1998 Large-scale screening for developmental genes in embryonic stem cells and embryoid bodies using retroviral entrapment vectors. Dev. Dyn. 212(2):181–197.