We spend about one‑third of our lives sleeping—or at least we should. Not getting enough sleep can have serious health consequences and is linked to high blood pressure, heart disease, and stroke.
Sleep deprived
A study by the American Sleep Apnea Association found that 70 percent of Americans report too little sleep at least one night a month, and 11 percent report inadequate sleep every night. Over time, this can take a major toll on mental and physical health. Now a new study says it may also increase the risk of eye disease.
The study, published in Stem Cell Reports, examined how sleep deprivation affects corneal stem cells. These cells are essential for replacing damaged or diseased cells in the cornea—the transparent layer that covers and protects the eye.
Researchers Wei Li, Zugou Liu, and colleagues from Xiamen University and Harvard Medical School found that short‑term sleep deprivation in mice increased the rate at which corneal stem cells multiplied. Producing too many new cells led to vision problems.
Connection with vision loss
They also found that long‑term sleep deprivation had an even greater impact. Sleep‑deprived mice had fewer active stem cells and were less able to replace damaged cells. That led to corneal thinning and a loss of transparency in remaining cells.
The findings suggest that sleep deprivation negatively affects the stem cells in the cornea, possibly leading to vision impairment in the long run. It’s not clear if these findings also apply to people, but if they do, the implications could be enormous.
The California Institute for Regenerative Medicine (CIRM) is also heavily involved in searching for treatments for diseases or conditions that affect vision. We have invested almost $150 million in funding 31 projects on vision loss including a clinical trial with UCLA’s Dr. Sophie Deng targeting the cornea, and other clinical trials for age-related macular degeneration and retinitis pigmentosa.
Shared with permission from International Society for Stem Cell Research. Read the source release here.
Sleep loss in short duration and longer duration have potential effect to disturb the metabolism equilibrium and hormones regulation of the body. Sleep deprivation causes oxidative stress in most of the cells and tissues. Oxidation damage of DNA reflects either impairment of repair mechanisms or increased rate of DNA damage that outstrips repairing. The incomplete antioxidant protection results in injured cells that then would either be repaired or die. Sleep loss induced inappropriate activation of immune system or immune -related dysfunction perse, but as response to cell injury. These signs include increases in circulating proinflammatory cytokines (IL-1β & IL-6),markers of cell stress or cytoprtection (inducible heme-oxygenase & heat shock proteins), changes in antioxidants enzymes, neutrophilia and neutrophil migration into tissues. Evidence of DNA damage in the brain has been reported in laboratory rodents with partially sleep deprived. Sleep loss caused increases in cell injury, death and hence accelerates cell proliferation. This is supported by the finding that increased in cell injury of intestinal was associated with increased in cell proliferation and death. However, restoration by sleep included biochemical and molecular events that restored balance and lower the rate of cell injury.
Current investigation showed that short-term of sleep deprived (SD) of mice induced hyperproliferation of cornea epithelial cells(CEPCs). This was followed by elevated levels of tear ROS and drastically drop of antioxidants capacity in tear and CEPCs of SD mice. There was no significant changes of GSH in TF, but decrease of GSH in CEPCs. The addition of exogenous H2O2 in low dose caused defect and apoptotic in epithelial but not obvious in CEPCs. However, low concentrations of H2O2 promoted expansion of CPCs. These results indicated different types of cell have different requirement of ROS to cause injury, death and proliferation of cells. Therefore, restoration of sleep tend to downregulate of end-point damage to lipids, proteins and DNA. In addition, an absence of any increases in cell burdens, such as production of new cells or imbalance of DNA damage and repair. Thus, the administration of L-glutathione eye drop may substantially improve the pathological symptoms for short-term of SD. This is in contrast to long-term of SD that showed cornea of eyes was less transparent, ocular surface became rough and dry. The arrangement of cornea basal epithelial cells was irregular and the thickness of cornea epithelial was decreased. This phenomenon was so called limbal stem cell deficiency diseases (lSCD), a sign of cornea conjuctivalization caused reducing of stemness in CEPCs. Cell based therapy is high recommended to improve the vision of patients with long-term SD.