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Photonic control of ligand nanospacing in self-assembly regulates stem cell fate.

ABSTRACT: Extracellular matrix (ECM) undergoes dynamic inflation that dynamically changes ligand nanospacing but has not been explored. Here we utilize ECM-mimicking photocontrolled supramolecular ligand-tunable Azo⁺ self-assembly composed of azobenzene derivatives (Azo⁺) stacked via cation-π interactions and stabilized with RGD ligand-bearing poly(acrylic acid). Near-infrared-upconverted-ultraviolet light induces cis-Azo⁺-mediated inflation that suppresses cation-π interactions, thereby inflating liganded self-assembly. This inflation increases nanospacing of "closely nanospaced" ligands from 1.8 nm to 2.6 nm and the surface area of liganded self-assembly that facilitate stem cell adhesion, mechanosensing, and differentiation both in vitro and in vivo, including the release of loaded molecules by destabilizing water bridges and hydrogen bonds between the Azo⁺ molecules and loaded molecules. Conversely, visible light induces trans-Azo⁺ formation that facilitates cation-π interactions, thereby deflating self-assembly with "closely nanospaced" ligands that inhibits stem cell adhesion, mechanosensing, and differentiation. In stark contrast, when ligand nanospacing increases from 8.7 nm to 12.2 nm via the inflation of self-assembly, the surface area of "distantly nanospaced" ligands increases, thereby suppressing stem cell adhesion, mechanosensing, and differentiation. Long-term in vivo stability of self-assembly via real-time tracking and upconversion are verified. This tuning of ligand nanospacing can unravel dynamic ligand-cell interactions for stem cell-regulated tissue regeneration.

SUBMITTER: Lee S

PROVIDER: S-EPMC10859239 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature

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Photonic control of ligand nanospacing in self-assembly regulates stem cell fate.

Lee Sungkyu S Yoo Jounghyun J Bae Gunhyu G Thangam Ramar R Heo Jeongyun J Park Jung Yeon JY Choi Honghwan H Kim Chowon C An Jusung J Kim Jungryun J Mun Kwang Rok KR Shin Seungyong S Zhang Kunyu K Zhao Pengchao P Kim Yuri Y Kang Nayeon N Han Seong-Beom SB Kim Dahee D Yoon Jiwon J Kang Misun M Kim Jihwan J Yang Letao L Karamikamkar Solmaz S Kim Jinjoo J Zhu Yangzhi Y Najafabadi Alireza Hassani AH Song Guosheng G Kim Dong-Hwee DH Lee Ki-Bum KB Oh Soong Ju SJ Jung Hyun-Do HD Song Hyun-Cheol HC Jang Woo Young WY Bian Liming L Chu Zhiqin Z Yoon Juyoung J Kim Jong Seung JS Zhang Yu Shrike YS Kim Yongju Y Jang Ho Seong HS Kim Sehoon S Kang Heemin H

Bioactive materials 20231226

Extracellular matrix (ECM) undergoes dynamic inflation that dynamically changes ligand nanospacing but has not been explored. Here we utilize ECM-mimicking photocontrolled supramolecular ligand-tunable Azo+ self-assembly composed of azobenzene derivatives (Azo+) stacked via cation-π interactions and stabilized with RGD ligand-bearing poly(acrylic acid). Near-infrared-upconverted-ultraviolet light induces cis-Azo+-mediated inflation that suppresses cation-π ...[more]

PMID: 38343773

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Project description:Our understanding on how selective mitochondrial autophagy, or mitophagy, can sustain the archetypal properties of stem cells is incomplete. PTEN-induced putative kinase 1 (PINK1) plays a key role in the maintenance of mitochondrial morphology and function and in the selective degradation of damaged mitochondria by mitophagy. Here, using embryonic fibroblasts fromPINK1 gene-knockout (KO) mice, we evaluated whether mitophagy is a causal mechanism for the control of cell-fate plasticity and maintenance of pluripotency. Loss of PINK1-dependent mitophagy was sufficient to dramatically decrease the speed and efficiency of induced pluripotent stem cell (iPSC) reprogramming. Mitophagy-deficient iPSC colonies, which were characterized by a mixture of mature and immature mitochondria, seemed unstable, with a strong tendency to spontaneously differentiate and form heterogeneous populations of cells. Although mitophagy-deficient iPSC colonies normally expressed pluripotent markers, functional monitoring of cellular bioenergetics revealed an attenuated glycolysis in mitophagy-deficient iPSC cells. Targeted metabolomics showed a notable alteration in numerous glycolysis- and TCA-related metabolites in mitophagy-deficient iPSC cells, including a significant decrease in the intracellular levels of α-ketoglutarate -a key suppressor of the differentiation path in stem cells. Mitophagy-deficient iPSC colonies exhibited a notably reduced teratoma-initiating capacity, but fully retained their pluripotency and multi-germ layer differentiation capacity in vivo. PINK1-dependent mitophagy pathway is an important mitochondrial switch that determines the efficiency and quality of somatic reprogramming. Mitophagy-driven mitochondrial rejuvenation might contribute to the ability of iPSCs to suppress differentiation by directing bioenergetic transition and metabolome remodeling traits. These findings provide new insights into how mitophagy might influence the stem cell decisions to retain pluripotency or differentiate in tissue regeneration and aging, tumor growth, and regenerative medicine.

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Photonic control of ligand nanospacing in self-assembly regulates stem cell fate.

Publications

Photonic control of ligand nanospacing in self-assembly regulates stem cell fate.

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