A5021815318- Barrier Structure and Function Studies
- Hippo pathway signaling and YAP/TAZ
- Intracerebral and Subarachnoid Hemorrhage Research
- Vascular Malformations Diagnosis and Treatment
- Intracranial Aneurysms: Treatment and Complications
- Cancer-related molecular mechanisms research
- Cancer-related gene regulation
- Kruppel-like factors research
- Connexins and lens biology
- Phagocytosis and Immune Regulation
- Wnt/β-catenin signaling in development and cancer
- Neurological diseases and metabolism
- Renal and related cancers
- Ferroptosis and cancer prognosis
- Hedgehog Signaling Pathway Studies
- Neurological Disease Mechanisms and Treatments
- Protist diversity and phylogeny
University of California, San Diego
2022-2025
Center for Research and Advanced Studies of the National Polytechnic Institute
2016-2022
Instituto Politécnico Nacional
2016-2021
Cerebral cavernous malformations (CCMs) are neurovascular lesions caused by loss of function mutations in 1 3 genes, including
BACKGROUND: Heterogeneity in the severity of cerebral cavernous malformations (CCMs) disease, including brain bleedings and thrombosis that cause neurological disabilities patients, suggests environmental, genetic, or biological factors act as disease modifiers. Still, underlying mechanisms are not entirely understood. Here, we report mild hypoxia accelerates CCM by promoting angiogenesis, neuroinflammation, vascular brains mouse models. METHODS: We used genetic studies, RNA sequencing,...
Renal compensatory hypertrophy (RCH) restores normal kidney function after disease or loss of tissue and is characterized by an increase in organ size due to cell enlargement not proliferation. In MDCK renal epithelial cells, silencing the tight junction protein zona occludens 2 (ZO-2 KD) induces two mechanisms: prolonging time that cells spend at G1 phase cycle cyclin D1 level, augmenting rate synthesis. The latter triggered nuclear accumulation increased transcriptional activity...
Endothelial cells respond to forces generated by laminar blood flow with changes in vasodilation, anticoagulant, fibrinolytic, or anti-inflammatory functions which preserve vessel patency. These responses sheer stress are primarily mediated the modulation of transcription factors Krüppel-like 2 and 4 (KLF2 KLF4). Notably, disturbed patterns, found vascular areas predisposed atherosclerosis, significantly reduce endothelial expression KLF2 KLF4, resulting transcriptome that exacerbate...
Endothelial cells respond to forces generated by laminar blood flow with changes in vasodilation, anticoagulant, fibrinolytic, or anti-inflammatory functions which preserve vessel patency. These responses shear stress are primarily mediated the modulation of following transcription factors: Krüppel-like factors 2 and 4 (KLF2 KLF4). Notably, disturbed patterns, found vascular areas predisposed atherosclerosis, significantly reduce endothelial expression KLF2 KLF4, resulting transcriptome that...
The presence of tight junction protein zonula occludens 2 (ZO-2) at the nucleus inhibits transcription genes regulated by TEAD factor. Here, we analyzed whether movement ZO-2 into modulates nuclear concentration TEAD. In sparse cultures knockdown Madin-Darby canine kidney cells, was diminished, as in parental cells transfected with a construct without localization signals, indicating that facilitates entry nucleus. Inhibition nPKCδ triggers interaction between and cytoplasm TEAD/ZO-2 complex...
ZO-2 is a peripheral tight junction (TJ) protein whose silencing in renal epithelia induces cell hypertrophy. Here, we found that KD MDCK cells, compensatory hypertrophy triggered rats by unilateral nephrectomy and liver steatosis of obese Zucker (OZ) rats, accompanied the diminished activity LATS, kinase Hippo pathway, nuclear concentration YAP, final effector this signaling route. appears to function as scaffold for pathway it associates LATS1. hypertrophic tissue due abundance mRNA, Sp1...
Cerebral Cavernous Malformations (CCMs) are neurovascular abnormalities in the central nervous system (CNS) caused by loss of function mutations KRIT1 (CCM1), CCM2, or PDCD10 (CCM3) genes. One most common symptoms CCM patients is associated with motor disability, weakness, seizures, stress, and anxiety, extent symptom may be due to location lesion within CNS whether multiple lesions present. Previous studies have primarily focused on understanding pathology using animal models. However, more...
MAGUK protein ZO-2 is present at tight junctions (TJs) and nuclei. In MDCK knockdown (KD) cells, nuclei exhibit an irregular shape with lobules indentations. This condition correlates increase in DNA double strand breaks, however cells are not senescent instead become resistant to UV-induced senescence. The nuclear also observed isolated those without TJs, due the lack of extracellular calcium. aberrant KD accompanied by a reduced expression lamins A/C B lamin receptors. Instead, it involves...
Abstract Background Cerebral Cavernous Malformations (CCMs) are neurovascular lesions caused by loss-of-function mutations in one of three genes, including KRIT1 (CCM1), CCM2, and PDCD10 (CCM3). CCMs affect ∼1/200 children adults, no pharmacologic therapy is available. CCM lesion count, size, aggressiveness vary widely among patients similar ages with the same mutation or even within members family. However, what determines transition from quiescent into mature active (aggressive) unknown....