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Academia Sinica highly values academic freedom and freedom of speech and encourages our colleagues to provide opinions on and propose solutions to key social issues. Nonetheless, research findings and opinions expressed independently by our colleagues do not necessarily reflect the official position of Academia Sinica. We expect all colleagues to adhere to academic norms and take responsibility by citing sources and ensuring accuracy when publishing independently. Research findings and opinions provided on behalf of Academia Sinica should be published according to established procedures.

2024-12-12
  • Research Findings
  • Institute of Biomedical Sciences
Separate anterior paraventricular thalamus projections differentially regulate sensory and affective aspects of pain

Pain is a common yet complex phenomenon involving both physical sensations and emotional responses. While the basic understanding of pain has advanced, the brain mechanisms driving these responses remain unclear. A team led by Dr. Chien-Chang Chen from the Institute of Biomedical Sciences (IBMS), Academia Sinica, has made a significant breakthrough in understanding the neural basis of chronic pain. The study revealed that chronic pain activates specific neuronal populations in the anterior paraventricular nucleus of the thalamus (PVA). These neurons are responsible for processing either the sensory or emotional aspects of pain, with their activity changing based on the pain type. Stimulating these neurons led to tactile hypersensitivity and avoidance behaviors, while suppressing them alleviated pain. Additionally, these neurons send signals to the bed nucleus of the stria terminalis (BNST) and the nucleus accumbens (NAc), which independently regulate different pain-related behaviors. This research not only deepens our understanding of pain mechanisms but also paves the way for innovative chronic pain treatments that could significantly improve patients' quality of life. The research was conducted by Dr. Chien-Chang Chen and his lab members, including Dr. Selomon Assefa Mindaye (first author, a TIGP-INS alumnus) and Dr. Wei-Hsin Chen, in collaboration with IBMS investigators Dr. Shih-Yu Chen and Dr. Shih-Pin Yang, as well as Dr. Arthur Chun-Chieh Shih from the Institute of Information Science, Academia Sinica. The findings were published in Cell Reports on November 26, 2024.

2024-11-15
  • Research Findings
  • Biodiversity Research Center
Clostridium innocuum inactivates host gut progesterone and arrests ovarian follicular development

Levels of progesterone, an endogenous female hormone, increase after ovulation; progesterone is crucial in the luteal phase to maintain successful pregnancy and prevent early miscarriage. Both endogenous and exogenous progesterone are recycled between the liver and gut; thus, the gut microbiota regulate host progesterone levels by inhibiting enterohepatic progesterone circulation. A research team led by Dr. Yin-Ru Chiang at the Biodiversity Research Center, Academia Sinica, and Mei-Jou Chen at the College of Medicine, National Taiwan University, have identified Clostridium innocuum as a major species involved in gut progesterone metabolism in women with infertility. C. innocuum converts progesterone into the neurosteroid epipregnanolone (with negligible progestogenic activity). The study purified and characterized the corresponding enzyme, namely NADPH-dependent 5β-dihydroprogesterone reductase, which is highly oxygen sensitive and whose corresponding genes are prevalent in C. innocuum. Moreover, C. innocuum–administered female C57BL/6 mice (aged 7 weeks) exhibited decreased plasma progesterone levels (~35%). Clostridium-specific antibiotics (metronidazole) restored low plasma progesterone levels in these mice. Furthermore, prolonged C. innocuum administration (12 weeks) arrested ovarian follicular development in female mice. Cytological and histological analyses indicated that C. innocuum may cause luteal phase insufficiency and affect menstrual regularity. The research findings suggest C. innocuum as a causal factor of progesterone resistance in women taking progesterone. The research has been published on November 7, 2024 in Gut Microbes.

2024-10-23
  • Seminars & Lectures
  • Institute of Molecular Biology
HURP binding to the vinca domain of β-tubulin accounts for cancer drug resistance

Vinca alkaloids, a class of tubulin-binding agent, are widely used in treating cancer, yet the emerging resistance compromises their efficacy. Hepatoma up-regulated protein (HURP), a microtubule-associated protein displaying heighted expression across various cancer types, reduces cancer cells’ sensitivity to vinca-alkaloid drugs upon overexpression. However, the molecular basis behind this drug resistance remains unknown. An international research team led by Dr. Kuo-Chiang Hsia at the Institute of Molecular Biology, Academia Sinica, Dr. Su-Yi Tsai (Department of Life Science, National Taiwan University) and Dr. Yuta Shimamoto (National Institute of Genetics) discover a tubulin-binding domain within HURP, and establish its role in regulating microtubule growth. Cryo-EM analysis reveals interactions between HURP's tubulin-binding domain and the vinca domain on β-tubulin-the site targeted by vinca alkaloid drugs. Importantly, HURP competes directly with the vinorelbine, a vinca alkaloid-based chemotherapeutic agent, countering microtubule growth defects caused by vinorelbine both in vitro and in vivo. The research findings elucidate a mechanism driving drug resistance in HURP-overexpressing cancer cells and emphasize HURP tubulin-binding domain’s role in mitotic spindle assembly. This underscores its potential as a therapeutic target to improve cancer treatment. This research has been published on October 14, 2024 in Nature Communications.

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