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Biology subjects

Lima, K.

Publications and source records attributed to Lima, K..

2 recordsLinked to original sources

Immune Response of Transplanted Kidney Tissues Assembled from Organoid Building Blocks

The increasing scarcity of organs and the significant morbidity linked to dialysis requires the development of engineered kidney tissues from human-induced pluripotent stem cells. To accomplish this, integrative approaches that synergize scalable kidney organoid differentiation, tissue biomanufacturing, and comprehensive assessment of their immune response and host integration are essential. Here, we create engineered human kidney tissues composed of kidney organoid building blocks (OBBs) and transplant them into mice reconstituted with allogeneic human immune cells. We assess their host vascular integration, in vivo maturation, and their ability to trigger human immune responses. Tissue-infiltrating human immune cells are composed of effector T cells and innate cells. This immune infiltration leads to kidney tissue injury characterized by reduced microvasculature, enhanced kidney cell apoptosis, and a unique inflammatory gene signature comparable to kidney organ transplant rejection in humans. Upon treatment with the immunosuppressive agent Rapamycin, the induced immune response is greatly suppressed. Our model serves as a translational platform to study engineered kidney tissue immunogenicity and develop novel therapeutic targets for kidney rejection.

bioengineering↗

The PIP4K2 inhibitor THZ-P1-2 exhibits antileukemia activity by disruption of mitochondrial homeostasis and autophagy

Treatment of acute leukemia is challenging due to genetic heterogeneity between and even within patients. Leukemic stem cells (LSCs) are relatively drug-resistant and frequently lead to relapse. Their plasticity and capacity to adapt to extracellular stress, in which mitochondrial metabolism and autophagy play important roles, further complicates treatment. Genetic models of phosphatidylinositol-5-phosphate 4-kinase type 2 proteins (PIP4K2s) inhibition demonstrated the relevance of these enzymes in mitochondrial homeostasis and autophagic flux. Here, we uncover the cellular and molecular effects of THZ-P1-2, a pan-inhibitor of PIP4K2s, in acute leukemia cells. THZ-P1-2 reduced cell viability and induced DNA damage, apoptosis, loss of mitochondrial membrane potential, and accumulation of acidic vesicular organelles. Protein expression analysis revealed that THZ-P1-2 impaired autophagy flux. In addition, THZ-P1-2 induced cell differentiation and showed synergistic effects with venetoclax in resistant leukemic models. In primary leukemia cells, LC-MS/MS-based proteome analysis revealed that sensitivity to THZ-P1-2 was associated with mitochondrial metabolism, cell cycle, cell-of-origin, and the TP53 pathway. Minimal effects of THZ-P1-2 observed in healthy CD34+ cells suggested a favorable therapeutic window. Our study provides insight into pharmacological inhibition of PIP4Ks targeting mitochondrial homeostasis and autophagy shedding light on a new class of drugs for acute leukemias.

pharmacology and toxicology↗