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Robling, Alexander G., PhD

Education

  • St. Mary's College of Maryland, BA, 1992
  • George Washington University, MA, 1995
  • University of Missouri - Columbia, PhD, 1998
  • Indiana University School of Medicine, Postdoctoral Fellowship, 1999-2001

 

Academic Appointments

  • 1999 Postdoctoral Fellow, Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN.
  • 2001 Assistant Scientist, Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN.
  • 2003 Assistant Scientist, Department of Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN.
  • 2003 Graduate Faculty, Indiana University School of Medicine
  • 2004 Assistant Professor, Department of Anatomy & Cell Biology, Indiana University School of Medicine, Indianapolis, IN.
  • 2007 Graduate Faculty, Purdue University, West Lafayette, IN.
  • 2008 Assistant Professor (adjunct), Department of Biomedical Engineering, Indiana University/Purdue University at Indianapolis (IUPUI), Indianapolis, IN.
  • 2010 Associate Professor (with tenure), Department of Anatomy & Cell Biology, Indiana University School of Medicine; and Department of Biomedical Engineering, IUPUI, Indianapolis, IN.

 

My laboratory works on treatments for metabolic and genetic bone diseases.  We use molecular genetic approaches in rodents to identify new ways to make bone stronger.  One particular approach that we have focused on is mechanobiology.  Mechanobiology merges the older science of mechanics with the newer and emerging disciplines of molecular biology and genetics.  At the center of mechanobiology is the cellular process of mechanotransduction, or the way cells sense and respond to mechanical forces.  We research how mechanical loads signal bone cells to build stronger bones.  Our research program has led us to the Wnt signaling pathway as a major regulator of mechanotransduction.  Current projects are centered around the particular steps in the Wnt cascade that are activated by mechanical stimuli and ultimately lead to increased anabolism.  

 

ASBMR_poster_Sost_Dkk1_rev7.jpg

Robling AG, Kang KS, Bullock WA, Foster WH, Murugesh D, Loots GG, Genetos DC. Sost, independent of the non-coding enhancer ECR5, is required for bone mechanoadaptation.  Bone. 2016 Nov;92:180-188. doi: 10.1016/j.bone.2016.09.001.  PMID: 27601226

 Jacobsen CM, Schwartz MA, Roberts HJ, Lim KE, Spevak L, Boskey AL, Zurakowski D, Robling AG, Warman ML. Enhanced Wnt signaling improves bone mass and strength, but not brittleness, in the Col1a1(+/mov13) mouse model of type I Osteogenesis Imperfecta.  Bone. 2016 Sep;90:127-32. doi:   0.1016/j.bone.2016.06.005.  PMID: 27297606

 Kedlaya R, Kang KS, Hong JM, Bettagere V, Lim KE, Horan D, Divieti-Pajevic P, Robling AG. Adult-Onset Deletion of β-Catenin in (10kb)Dmp1-Expressing Cells Prevents Intermittent PTH-Induced Bone Gain.  Endocrinology. 2016 Aug;157(8):3047-57. doi: 10.1210/en.2015-1587.  PMID: 27253995

 Kang KS, Hong JM, Robling AG. Postnatal β-catenin deletion from Dmp1-expressing osteocytes/osteoblasts reduces structural adaptation to loading, but not periosteal load-induced bone formation.  Bone. 2016 Jul;88:138-45. doi: 10.1016/j.bone.2016.04.028.  MID: 27143110

 Collette NM, Yee CS, Hum NR, Murugesh DK, Christiansen BA, Xie L, Economides AN, Manilay JO, Robling AG, Loots GG. Sostdc1 deficiency accelerates fracture healing by promoting the expansion of periosteal mesenchymal stem cells.  Bone. 2016 Jul;88:20-30. doi: 10.1016/j.bone.2016.04.005.  PMID: 27102547 Free Article

 Alam I, Alkhouli M, Gerard-O'Riley RL, Wright WB, Acton D, Gray AK, Patel B, Reilly AM, Lim KE, Robling AG, Econs MJ.  Osteoblast-Specific Overexpression of Human WNT16 Increases Both Cortical and Trabecular Bone Mass and Structure in Mice.  Endocrinology. 2016 Feb;157(2):722-36. doi: 10.1210/en.2015-1281.  PMID: 26584014

Department of Anatomy & Cell Biology | IU School of Medicine | 635 Barnhill Drive, MS 5035 | Indianapolis, IN 46202 | (317) 274-7494