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Institution-verified
Presence
Current · Arkansas
Last published
2026
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Institutional record
Refreshed
2026-10-09
R
Roy Morello
Sourced from institutional research profiles (UAMS TRI or ARA).
Federal Grant PI
High Impact
Professor
Also affiliated: Harvard University (2002); Baylor University (2006); Baylor College of Medicine (2001–2010); Boys Town National Research Hospital (2002)
29 h-index
75 pubs
4,067 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Roy Morello's research focuses on the molecular mechanisms underlying genetic bone disorders, particularly osteogenesis imperfecta (OI). He has investigated the roles of specific proteins, such as CRTAP and Type X collagen, in bone development and the consequences of their mutations. His work has identified CRTAP as essential for prolyl 3-hydroxylation, a process critical for collagen function, and linked mutations in CRTAP and LEPRE1 to recessive forms of OI. Additionally, his research has explored the regulation of Type X collagen gene expression by Runx2, contributing to its specific expression in hypertrophic chondrocytes.
Morello's laboratory has utilized mouse models to study these conditions, including knockout mice, to understand the in vivo effects of genetic deficiencies. His investigations have also extended to related genetic disorders, such as mutations in SERPINF1 causing osteogenesis imperfecta type VI, and the role of LMX1B in regulating glomerular basement membrane collagen expression, which is relevant to renal disease in nail patella syndrome. He has received federal funding from the NIH/National Heart Lung and Blood Institute for research into lung developmental defects caused by type I collagen mutations in mouse models of OI.
With an h-index of 30 and over 4,100 citations across 79 publications, Morello is recognized as a high-impact researcher. He actively collaborates with colleagues at the University of Arkansas for Medical Sciences, including Milena Dimori, Charles A. O’Brien, Jeff D. Thostenson, and Luke Sultana, with whom he has co-authored multiple publications. His ongoing work continues to advance the understanding of skeletal dysplasias and associated pathologies.
Metrics
- h-index: 29
- Publications: 75
- Citations: 4,067
Positions
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Professor 2009–presentUniversity of Arkansas for Medical Sciences Physiology Institutional directory
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Post-Doc/Assistant Professor 1998–2009Baylor College of Medicine Molecular and Human Genetics ORCID
Selected Publications
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C107-24 Gata6 and Tcf21: A Yin-Yang Axis Balancing Matrix Integrity and Lipogenic Potential in Alveolar Fibroblasts (2026)
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B74-07 Respiratory Manifestations in Ehlers-Danlos Syndrome and Generalized Hypermobility Spectrum Disorder: Meeting Report and Future Considerations (2026)
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Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function (2026)
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Impact of short-term housing temperature alteration on metabolic parameters and adipose tissue in female mice (2025)
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A new Col1a1 conditional knock-in mouse model to study osteogenesis imperfecta (2024)
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A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta (2024)
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The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice (2023)
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A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation (2023)
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Discovery of small molecule agonists of the Relaxin Family Peptide Receptor 2 (2022)
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Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta (2022)
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RXFP2 Small Molecule Agonists: Potential Therapeutics for Osteoporosis (2022)
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Haploinsufficiency of Col5a1 causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome (2022)
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The Osteocyte Transcriptome: Discovering Messages Buried Within Bone (2021)
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Management of Endocrine Disease: Osteogenesis imperfecta: an update on clinical features and therapies (2020)
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Dental and craniofacial defects in the Crtap−/− mouse model of osteogenesis imperfecta type VII (2020)
Federal Grants 1 $380,533 total
NIH
Contact PI
Sep 2023 - Jul 2027
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Lung alterations in recessive Osteogenesis Imperfecta due to loss of the prolyl 3-hydroxylation complex UAMS 2018 Medical Research Endowment award
- Defining the role of post-translational regulation by extracellular proteases in the pathogenesis of Staphylococcus aureus osteomyelitis NIH
- Elucidating the role of type I collagen mutations on respiratory function in osteogenesis imperfecta. American Lung Association
- Elucidating the role of type I collagen mutations on respiratory function in osteogenesis imperfecta American Lung Association
- Respiratory Function in Animal Models of Skeletal Dysplasias UAMS Research Scholar Pilot Grant Award in Child Health
- Matrix-mediated effects on Bone Marrow Stromal Cells (BMSCs) UAMS 2012 Medical Research Endowment award
- Primary lung defects in mouse models of osteogenesis imperfecta NIH/Nat. Inst. of Child Health & Human Development
- Sc65, a novel osteoporosis related gene ASBMR Junior Faculty Osteoporosis Research Award
- Crtap function during skeletal homeostasis NIH
- Role of the Leprecan Genes in Skeletal Formation NIH
- Morello Startup UAMS College of Medicine
- Targeted Enzyme Replacement Therapy for Rare Forms of Osteogenesis Imperfecta NIH
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences
- Role of collagen prolyl 3-hydroxylation in Osteogenesis imperfecta OSTEOGENESIS IMPERFECTA FOUNDATION - Michael Geisman Research Fellowship
Collaboration Network
Top Collaborators
Milena Dimori
University of Arkansas for Medical Sciences
14 shared publications
In database
- Sc65-Null Mice Provide Evidence for a Novel Endoplasmic Reticulum Complex Regulating Collagen Lysyl Hydroxylation
- P3h3-null and Sc65-null Mice Phenocopy the Collagen Lysine Under-hydroxylation and Cross-linking Abnormality of Ehlers-Danlos Syndrome Type VIA
- Sc65 Is a Novel Endoplasmic Reticulum Protein That Regulates Bone Mass Homeostasis
- The Osteocyte Transcriptome Is Extensively Dysregulated in Mouse Models of Osteogenesis Imperfecta
- Loss of RANKL in osteocytes dramatically increases cancellous bone mass in the osteogenesis imperfecta mouse (oim)
Showing 5 of 14 shared publications
John L. Carroll
University of Arkansas for Medical Sciences
6 shared publications
In database
- Respiratory defects in the CrtapKO mouse model of osteogenesis imperfecta
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- Haploinsufficiency of Col5a1 causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome
- A new Col1a1 conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
Showing 5 of 6 shared publications
David R. Eyre
University of Washington (US)
5 shared publications
- Sc65-Null Mice Provide Evidence for a Novel Endoplasmic Reticulum Complex Regulating Collagen Lysyl Hydroxylation
- P3h3-null and Sc65-null Mice Phenocopy the Collagen Lysine Under-hydroxylation and Cross-linking Abnormality of Ehlers-Danlos Syndrome Type VIA
- Sc65 Is a Novel Endoplasmic Reticulum Protein That Regulates Bone Mass Homeostasis
- Differential Effects of Collagen Prolyl 3-Hydroxylation on Skeletal Tissues
- Severe osteogenesis imperfecta caused by a small in‐frame deletion in CRTAP
Charles A. O’Brien
Central Arkansas Veterans Healthcare System
5 shared publications
In database
- Loss of RANKL in osteocytes dramatically increases cancellous bone mass in the osteogenesis imperfecta mouse (oim)
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Modeling Rare Bone Diseases in Animals
- A new Col1a1 conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
Larry J. Suva
Texas A&M University (US)
4 shared publications
- Sc65-Null Mice Provide Evidence for a Novel Endoplasmic Reticulum Complex Regulating Collagen Lysyl Hydroxylation
- Sc65 Is a Novel Endoplasmic Reticulum Protein That Regulates Bone Mass Homeostasis
- Extensive Remineralization of Large Pelvic Lytic Lesions Following Total Therapy Treatment in Patients With Multiple Myeloma
- Re-Mineralization of Large Pelvic Lytic Lesions By CT Imaging in Patients with Multiple Myeloma: The Arkansas Experience
Sarah M. Zimmerman
University of Arkansas for Medical Sciences (US)
4 shared publications
- Sc65-Null Mice Provide Evidence for a Novel Endoplasmic Reticulum Complex Regulating Collagen Lysyl Hydroxylation
- The Osteocyte Transcriptome Is Extensively Dysregulated in Mouse Models of Osteogenesis Imperfecta
- Loss of RANKL in osteocytes dramatically increases cancellous bone mass in the osteogenesis imperfecta mouse (oim)
- Expression characterization and functional implication of the collagen-modifying Leprecan proteins in mouse gonadal tissue and mature sperm
Melissa E. Heard‐Lipsmeyer
University of Arkansas for Medical Sciences (US)
4 shared publications
- The Osteocyte Transcriptome Is Extensively Dysregulated in Mouse Models of Osteogenesis Imperfecta
- Loss of RANKL in osteocytes dramatically increases cancellous bone mass in the osteogenesis imperfecta mouse (oim)
- Respiratory defects in the CrtapKO mouse model of osteogenesis imperfecta
- Expression characterization and functional implication of the collagen-modifying Leprecan proteins in mouse gonadal tissue and mature sperm
Jeff D. Thostenson
University of Arkansas for Medical Sciences
4 shared publications
In database
- Loss of RANKL in osteocytes dramatically increases cancellous bone mass in the osteogenesis imperfecta mouse (oim)
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- A new Col1a1 conditional knock-in mouse model to study osteogenesis imperfecta
- Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function
Roberta Besio
University of Arkansas for Medical Sciences (US)
3 shared publications
- Sc65-Null Mice Provide Evidence for a Novel Endoplasmic Reticulum Complex Regulating Collagen Lysyl Hydroxylation
- Sc65 Is a Novel Endoplasmic Reticulum Protein That Regulates Bone Mass Homeostasis
- Expression characterization and functional implication of the collagen-modifying Leprecan proteins in mouse gonadal tissue and mature sperm
Frances L. Swain
University of Arkansas for Medical Sciences (US)
3 shared publications
- Sc65-Null Mice Provide Evidence for a Novel Endoplasmic Reticulum Complex Regulating Collagen Lysyl Hydroxylation
- Sc65 Is a Novel Endoplasmic Reticulum Protein That Regulates Bone Mass Homeostasis
- Expression characterization and functional implication of the collagen-modifying Leprecan proteins in mouse gonadal tissue and mature sperm
Dana Gaddy
University of Arkansas for Medical Sciences (US)
3 shared publications
- Impact of sarA and Phenol-Soluble Modulins on the Pathogenesis of Osteomyelitis in Diverse Clinical Isolates of Staphylococcus aureus
- Sc65 Is a Novel Endoplasmic Reticulum Protein That Regulates Bone Mass Homeostasis
- Expression characterization and functional implication of the collagen-modifying Leprecan proteins in mouse gonadal tissue and mature sperm
Erica P. Homan
Baylor College of Medicine (US)
3 shared publications
- Mutations in SERPINF1 cause osteogenesis imperfecta type VI
- Differential Effects of Collagen Prolyl 3-Hydroxylation on Skeletal Tissues
- Recessive Osteogenesis Imperfecta Due to Mutations in CRTAP, LEPRE1 and PPIB
Frank Rauch
McGill University (CA)
3 shared publications
- Mutations in SERPINF1 cause osteogenesis imperfecta type VI
- Severe osteogenesis imperfecta caused by a small in‐frame deletion in CRTAP
- Role of Cartilage-Associated Protein in Skeletal Development
MaryAnn Weis
University of Washington (US)
3 shared publications
- Sc65-Null Mice Provide Evidence for a Novel Endoplasmic Reticulum Complex Regulating Collagen Lysyl Hydroxylation
- P3h3-null and Sc65-null Mice Phenocopy the Collagen Lysine Under-hydroxylation and Cross-linking Abnormality of Ehlers-Danlos Syndrome Type VIA
- Severe osteogenesis imperfecta caused by a small in‐frame deletion in CRTAP
Brendan Lee
Baylor College of Medicine (US)
3 shared publications
- Mutations in SERPINF1 cause osteogenesis imperfecta type VI
- P3h3-null and Sc65-null Mice Phenocopy the Collagen Lysine Under-hydroxylation and Cross-linking Abnormality of Ehlers-Danlos Syndrome Type VIA
- Recessive Osteogenesis Imperfecta Due to Mutations in CRTAP, LEPRE1 and PPIB
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