M M O'Mara studies how certain proteins in the body contribute to inflammatory arthritis, especially rheumatoid arthritis. One significant area of their research looks at the protein CD13, which leaks into the bloodstream and can activate receptors on immune and joint cells, leading to inflammation. They aim to understand how these mechanisms work and explore potential treatments that could block this process, providing new options for people suffering from arthritis and other inflammatory diseases.
Key findings
The protein CD13 activates the B1 receptors on immune cells, leading to inflammation in arthritis.
In rheumatoid arthritis patients, B1 receptors are found to be overactive, contributing to disease symptoms.
Blocking the B1 receptor in both human tissue samples and mouse models effectively stopped the inflammation.
Frequently asked questions
Does Dr. M M O'Mara study arthritis?
Yes, Dr. O'Mara specifically studies inflammatory arthritis, including rheumatoid arthritis.
What treatments has Dr. M M O'Mara researched?
Dr. O'Mara's research suggests that blocking the B1 receptor could serve as a new treatment target for rheumatoid arthritis.
Is Dr. M M O'Mara's work relevant to patients with rheumatoid arthritis?
Yes, their work is highly relevant as it explores new ways to treat rheumatoid arthritis by targeting specific proteins involved in inflammatory processes.
Publications in plain English
A single-cell transposable element atlas of human cell identity.
2025
Cell reports methods
Reyes-Gopar H, Marston JL, Singh B, Greenig M, Lin J +13 more
Plain English This research studied how transposable elements (TEs), a type of DNA sequence, function in human cells using a new tool called Stellarscope, which helps analyze single-cell RNA data more effectively. The researchers found that TEs can help identify different cell types and specific cell groups that traditional methods miss. This is important because it improves our understanding of human biology on a cellular level, which could lead to better insights into health and disease.
Who this helps: This benefits researchers and doctors working to understand cell biology and develop new treatments.
Dopkins N, Singh B, Michael S, O'Mara MM, Marston JL +3 more
Plain English This study explored how certain parts of our DNA, called retrotransposons, interact with our immune system when the body detects harmful bacteria. The researchers found that when the immune system was activated by a bacterial signal, a significant increase in the production of retrotransposons occurred, which led to higher levels of inflammation, specifically measured by the cytokine TNF-alpha. They discovered that using a reverse transcriptase inhibitor reduced this inflammation response, indicating a new way our body’s DNA can influence how we respond to infections and regulatory mechanisms.
Who this helps: This benefits patients with inflammatory conditions linked to infections and their doctors looking for new treatment options.
A single-cell transposable element atlas of human cell identity.
2023
bioRxiv : the preprint server for biology
Reyes-Gopar H, Marston JL, Singh B, Greenig M, Lin J +13 more
Plain English This research focused on using a new tool called Stellarscope to analyze how certain genetic elements, known as transposable elements (TEs), are expressed in human immune cells. The study found that these TEs can help identify different cell types, revealing new cell groups that traditional methods missed. This is important because it enhances our understanding of human biology and could lead to better insights into diseases and treatments.
Who this helps: This benefits researchers studying immune cells and potentially patients with immune-related conditions.
How human endogenous retroviruses interact with the microbiota in health and disease.
2022
Trends in microbiology
Dopkins N, O'Mara MM, Singh B, Marston JL, Bendall ML +1 more
Plain English This study looked at how certain viruses in our bodies, called endogenous retroviruses, interact with the millions of microorganisms living in our digestive system, known as the microbiota. Researchers found that these retroviruses play a crucial role in communication between the body and the microbiota, which can affect our immune system. This research matters because it helps us understand how our health and disease states may be influenced by the relationship between these viruses and our microbiota.
Who this helps: This helps patients by providing insights into potential new treatments for immune-related diseases.
A field guide to endogenous retrovirus regulatory networks.
2022
Molecular cell
Dopkins N, O'Mara MM, Lawrence E, Fei T, Sandoval-Motta S +2 more
Plain English This study looked at how germ cells, which are involved in reproduction, manage infections from retroviruses that can insert their genetic material into the DNA of mammals. Researchers found that these inserted viral sequences, called endogenous retroviruses (ERVs), are not just leftover DNA; they play important roles in the body's function, but they need to be kept in check to avoid harming cells. Understanding how the body regulates these ERVs is important because it helps maintain healthy DNA and overall cellular function.
Who this helps: This helps researchers and scientists working on genetic health and developmental biology.
Functional Characterization of Glycoprotein Nonmetastatic Melanoma Protein B in Scleroderma Fibrosis.
2022
Frontiers in immunology
Palisoc PJ, Vaikutis L, Gurrea-Rubio M, Model EN, O'mara MM +5 more
Plain English This study looked at how a protein called GPNMB behaves in the skin cells of patients with diffuse cutaneous scleroderma (dcSSc), a condition that causes skin thickening. Researchers found that the levels of GPNMB were higher in skin cells from dcSSc patients compared to healthy individuals, with notable levels of its soluble form measured at 147.4 pg/ml versus 84.8 pg/ml. This protein appears to help reduce cell activity that leads to fibrosis, suggesting that boosting GPNMB could be a new way to treat scleroderma.
Who this helps: This benefits patients with scleroderma.
Soluble CD13 induces inflammatory arthritis by activating the bradykinin receptor B1.
2022
The Journal of clinical investigation
Tsou PS, Lu C, Gurrea-Rubio M, Muraoka S, Campbell PL +26 more
Plain English Researchers discovered that a protein called CD13, which leaks into the bloodstream, causes inflammatory arthritis by activating a receptor called B1R found on joint cells. They confirmed this by showing that blocking B1R with drugs stopped the inflammation in multiple types of arthritis in mice and in human joint tissue samples.
This matters because B1R could be a new drug target to treat rheumatoid arthritis and other inflammatory diseases by preventing CD13 from triggering joint inflammation.
Multicenter phase II trial of sunitinib in the treatment of nongastrointestinal stromal tumor sarcomas.
2009
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
George S, Merriam P, Maki RG, Van den Abbeele AD, Yap JT +11 more
Plain English This study looked at the effects of a drug called sunitinib on patients with advanced types of soft tissue sarcomas that are not gastrointestinal stromal tumors (non-GIST). Out of 53 patients treated, one person showed significant improvement, and 10 patients (20%) had their disease stabilize for at least 16 weeks. This is important because it shows that sunitinib can help some patients with these hard-to-treat tumors manage their condition better.
Who this helps: This benefits patients with advanced non-GIST sarcomas.