Publications by authors named "J F Giani"

Article Synopsis
  • - The study explored how early life stress from maternal separation and early weaning (MSEW) impacts blood pressure in obese male mice, focusing on the role of the renin-angiotensin-aldosterone system.
  • - Both control and MSEW mice on a high-fat diet showed similar increases in angiotensinogen levels, but there was no activation of the renin-angiotensin system in their fat or kidneys.
  • - Despite a reduction in blood pressure after treating with an angiotensin-converting enzyme inhibitor, MSEW mice still experienced heightened sympathetic tone, indicating that other mechanisms beyond angiotensin II contribute to their elevated blood pressure.
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Testis angiotensin-converting enzyme (tACE) plays a critical role in male fertility, but the mechanism is unknown. By using ACE C-domain KO (CKO) mice which lack tACE activity, we found that ATP in CKO sperm was 9.4-fold lower than WT sperm.

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The renin-angiotensin system (RAS) has been widely known as a circulating endocrine system involved in the control of blood pressure. However, components of RAS have been found to be localized in rather unexpected sites in the body including the kidneys, brain, bone marrow, immune cells, and reproductive system. These discoveries have led to steady, growing evidence of the existence of independent tissue RAS specific to several parts of the body.

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Aims: The metabolic failure of macrophages to adequately process lipid is central to the aetiology of atherosclerosis. Here, we examine the role of macrophage angiotensin-converting enzyme (ACE) in a mouse model of PCSK9-induced atherosclerosis.

Methods And Results: Atherosclerosis in mice was induced with AAV-PCSK9 and a high-fat diet.

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Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive disease with poor prognosis, which is mainly due to drug resistance. The biology determining the response to chemo-radiotherapy in HNSCC is poorly understood. Using clinical samples, we found that miR124-3p and miR766-3p are overexpressed in chemo-radiotherapy-resistant (non-responder) HNSCC, as compared to responder tumors.

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