Dataset Information

Chitooligosaccharide Maintained Cell Membrane Integrity by Regulating Reactive Oxygen Species Homeostasis at Wounds of Potato Tubers during Healing.

ABSTRACT: Chitooligosaccharide (COS) is a degradation product of chitosan. Although COS increased fruit resistance by regulating the metabolism of reactive oxygen species (ROS), few reports are available on whether COS regulates ROS homeostasis at wounds of potato tubers during healing. In this study, COS increased gene expression and activities of NADPH oxidase and superoxide dismutase, and promoted the generation of O₂^●- and H₂O₂. Moreover, COS increased gene expression and activities of catalase, peroxidase, and AsA-GSH cycle-related enzymes, as well as the levels of ascorbic acid and glutathione levels. In addition, COS elevated the scavenging ability of DPPH, ABTS⁺, and FRAP, and reduced cell membrane permeability and malondialdehyde content. Taken together, COS could maintain cell membrane integrity by eliminating excessive H₂O₂ and improving the antioxidant capacity in vitro, which contributes to the maintainance of cell membrane integrity at wounds of potato tubers during healing.

SUBMITTER: Xie P

PROVIDER: S-EPMC9495885 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature

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Chitooligosaccharide Maintained Cell Membrane Integrity by Regulating Reactive Oxygen Species Homeostasis at Wounds of Potato Tubers during Healing.

Xie Pengdong P Yang Yangyang Y Gong Di D Yu Lirong L Han Ye Y Zong Yuanyuan Y Li Yongcai Y Prusky Dov D Bi Yang Y

Antioxidants (Basel, Switzerland) 20220910 9

Chitooligosaccharide (COS) is a degradation product of chitosan. Although COS increased fruit resistance by regulating the metabolism of reactive oxygen species (ROS), few reports are available on whether COS regulates ROS homeostasis at wounds of potato tubers during healing. In this study, COS increased gene expression and activities of NADPH oxidase and superoxide dismutase, and promoted the generation of O2●- and H2O2. Moreover, COS increased gene ...[more]

PMID: 36139864

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Project description:This is a study to characterize gene expression profiles in stored Russet Burbank potato tubers. Tubers were harvested from commercial fields in the central sands region of Wisconsin in the fall of 2006. The tubers were put into storage at 55 degrees F for preconditioning and wound healing. Shortly after the temperature of the storage bin began to decrease, uniform, healthy tubers were selected for use in this microarray analysis. Tubers were at 53.6 degrees F at this time, and pieces of starch-storing tissue were collected for use as the reference sample. Other tubers were moved to temperature-controlled lockers and these were cooled gradually to either 48 or 40 degrees F following industry standard procedures. The expectation was that tubers held at 48 degrees would not have a significant accumulation of glucose and fructose, but that tubers cooled to 40 degrees would undergo low temperature sweetening and accumulate glucose and fructose to a degree that is unsuitable for processing. Three weeks later, when the locker temperatures were 48 degrees F and 41.5 degrees F, tissue samples were collected for RNA analysis. After another three weeks, samples were collected from tubers at 48 degrees F and 40 degrees F. At that time some tubers were moved from the 48 degree locker to the 40 degree locker in order to see if gene expression changes observed as a result of gradual cooling are similar to those that occur following a sudden decrease in temperature. Three weeks later, samples were collected from tubers held at 48 degrees F, tubers held at 40 degrees F, and from the tubers that were moved from 48 to 40 degrees F. At this time another set of tubers was transferred from 48 degrees to 40 degrees. Three weeks later the last samples were harvested from tubers held at 48 degrees F, from tubers held at 48 degrees F and from tubers that were transferred three weeks prior from 48 to 40 degrees. RNA was isolated from tissue extracted from three tubers. Keywords: Reference design

Project description:KRIT1 is a gene responsible for Cerebral Cavernous Malformations (CCM), a major cerebrovascular disease characterized by abnormally enlarged and leaky capillaries that predispose to seizures, focal neurological deficits, and fatal intracerebral hemorrhage. Comprehensive analysis of the KRIT1 gene in CCM patients has suggested that KRIT1 functions need to be severely impaired for pathogenesis. However, the molecular and cellular functions of KRIT1 as well as CCM pathogenesis mechanisms are still research challenges. We found that KRIT1 plays an important role in molecular mechanisms involved in the maintenance of the intracellular Reactive Oxygen Species (ROS) homeostasis to prevent oxidative cellular damage. In particular, we demonstrate that KRIT1 loss/down-regulation is associated with a significant increase in intracellular ROS levels. Conversely, ROS levels in KRIT1(-/-) cells are significantly and dose-dependently reduced after restoration of KRIT1 expression. Moreover, we show that the modulation of intracellular ROS levels by KRIT1 loss/restoration is strictly correlated with the modulation of the expression of the antioxidant protein SOD2 as well as of the transcriptional factor FoxO1, a master regulator of cell responses to oxidative stress and a modulator of SOD2 levels. Furthermore, we show that the KRIT1-dependent maintenance of low ROS levels facilitates the downregulation of cyclin D1 expression required for cell transition from proliferative growth to quiescence. Finally, we demonstrate that the enhanced ROS levels in KRIT1(-/-) cells are associated with an increased cell susceptibility to oxidative DNA damage and a marked induction of the DNA damage sensor and repair gene Gadd45alpha, as well as with a decline of mitochondrial energy metabolism. Taken together, our results point to a new model where KRIT1 limits the accumulation of intracellular oxidants and prevents oxidative stress-mediated cellular dysfunction and DNA damage by enhancing the cell capacity to scavenge intracellular ROS through an antioxidant pathway involving FoxO1 and SOD2, thus providing novel and useful insights into the understanding of KRIT1 molecular and cellular functions.

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Dataset Information

Chitooligosaccharide Maintained Cell Membrane Integrity by Regulating Reactive Oxygen Species Homeostasis at Wounds of Potato Tubers during Healing.

Publications

Chitooligosaccharide Maintained Cell Membrane Integrity by Regulating Reactive Oxygen Species Homeostasis at Wounds of Potato Tubers during Healing.

Similar Datasets

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