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About us
Our laboratory focuses on researching the pathogenesis of endometriosis and developing therapeutic strategies for this widespread cause of infertility and agonizing condition affecting women of fertile age worldwide. While endometriosis is highly prevalent, its exact etiology remains speculative, and current treatments aim to alleviate symptoms rather than targeting the root cause. We aim to investigate the impact of hypoxia-induced polarization of macrophages on endometriosis progression and explore the selective targeting of the M2 macrophage population using a proapoptotic m2pep KLA fusion peptide. Our research uniquely examines the endometriosis-macrophage crosstalk under hypoxic conditions in a tightly regulated environment, seeking to uncover critical molecular mechanisms underlying hypoxia-induced M2 activation in endometriotic pathogenesis. Through the use of physiologically relevant mice endometrial stromal cell culture (ESCC) and macrophage culture models, as well as human endometrial stromal cell culture, we aim to decipher the complex interactions involved. Validation of our findings will be conducted using in vivo endometriotic mice models and Human 3D endometrial organoid models. By elucidating the potential of a molecular-targeting approach for M2 macrophage depletion, our research strives to contribute to more effective treatment strategies and ultimately improve the management of endometriosis, addressing the unmet medical need in the field. Collaboration with researchers, clinicians, and institutions is highly encouraged to foster a comprehensive approach to endometriosis research, and the research is supported by grants from various funding agencies dedicated to advancing women's health.
Understanding the molecular mechanism of bidirectional interaction between activated macrophages and Neutrophil Extracellular Traps (NETs)
There is strong evidence that macrophages play a key role in the pathogenesis of Endometriosis. Numerous reports have suggested endometriosis-associated macrophages (EAM) play a key role in creating an immunosuppressive microenvironment facilitating the clinical manifestation. Because of the pivotal role that macrophages play in endometriosis, it is also termed a disease of macrophage. Another major immune cell population that is enriched in the endometriotic peritoneal milieu is neutrophil. However, the involvement of neutrophils in the pathology of endometriosis is yet to be fully understood. Neutrophils are regarded as the foot soldiers of the innate immune system as they act as first responders by phagocytosis and intracellular killing. In response to the presence of infection, neutrophils can eject a large web‐like structure of DNA coated with antimicrobial proteins that can trap and kill pathogens. This process is termed neutrophil extracellular traps (NETs) formation. NETs however can work as a double-edged sword, as they not only promote inflammation by various mechanisms but may also cause tissue injury. Elevated levels of peripheral plasma NET levels are seen in endometriotic patients. Although NETs and macrophages are found to colocalize in endometriotic lesions and peritoneal microenvironments, the impact of NETs on macrophage function or vice versa in the context of endometriosis is not fully understood. We aim to investigate the interaction of NETs and macrophages in the pathophysiological context of endometriosis in murine and human models.Artificial Intelligence augmented oocyte retrieval
The presence of endometriomas poses significant challenges during the in-vitro fertilization (IVF) process, making it difficult to collect oocytes from the ovary. Currently, there is no effective way to prevent accidental contamination of aspirated oocytes with endometriotic tissues while performing Transvaginal Oocyte Retrieval (TVOR) in endometriotic patients. To address this issue, we propose the development of a multispectral optoacoustic and ultrasound imaging-based smart needle guiding technology for oocyte retrieval. By integrating artificial intelligence (AI) and cutting-edge imaging techniques, our aim is to automate the oocyte retrieval process and minimize risk factors during assisted reproduction. The guided intervention involves identifying the boundaries of endometriomas and follicles with viable oocytes, which is enhanced by utilizing multispectral imaging with AI-assisted identification based on relevant clinical biomarkers. The real-time imaging information will then guide the interventionalist to avoid potential contamination of extracted oocytes. The proposed system will calculate the optimal trajectory to avoid touching the endometrioma and non-mature oocyte walls, providing visual assistance to the operator. The findings will be validated using standard laboratory protocols for IVF on the extracted oocytes.
Proapoptotic peptide mediated targeted depletion of Endometriosis Associated M2 macrophage population
Our laboratory focuses on researching the pathogenesis of endometriosis and developing therapeutic strategies for this widespread cause of infertility and agonizing condition affecting women of fertile age worldwide. While endometriosis is highly prevalent, its exact etiology remains speculative, and current treatments aim to alleviate symptoms rather than targeting the root cause. We aim to investigate the impact of hypoxia-induced polarization of macrophages on endometriosis progression and explore the selective targeting of the M2 macrophage population using a proapoptotic m2pep KLA fusion peptide. Our research uniquely examines the endometriosis-macrophage crosstalk under hypoxic conditions in a tightly regulated environment, seeking to uncover critical molecular mechanisms underlying hypoxia-induced M2 activation in endometriotic pathogenesis. Through the use of physiologically relevant mice endometrial stromal cell culture (ESCC) and macrophage culture models, as well as human endometrial stromal cell culture, we aim to decipher the complex interactions involved. Validation of our findings will be conducted using in vivo endometriotic mice models and Human 3D endometrial organoid models. By elucidating the potential of a molecular-targeting approach for M2 macrophage depletion, our research strives to contribute to more effective treatment strategies and ultimately improve the management of endometriosis, addressing the unmet medical need in the field. Collaboration with researchers, clinicians, and institutions is highly encouraged to foster a comprehensive approach to endometriosis research, and the research is supported by grants from various funding agencies dedicated to advancing women's health.
Research Focus
“Formal education will make you a living; self-education will make you a fortune.”
- Jim Rohn
