Studying the meibomian gland for years has led to an interesting idea which needs to be explored: how to regenerate the holocrine cells that have atrophied away at the base of each meibomian gland.
The new frontier in restoring the meibomian glands will be to inject adult stem cells into the meibomian gland and see if they will regenerate a new meibum-producing cell.
If it does, we could save millions of patients the misery of chronic eye pain.
We are launching such a study and invite you to contact me if you are interested. For more information email us for more information: ABlankenship@voeyedr.com
Here are some highlights from below paper:
The variation in cell-cycle rate that we found between each acinus, and between the acini and duct epithelium, suggests that they have distinct lineages that may operate on hierarchical cell-cycle programs.
Meibomian gland LRCs exist in lower populations and cycle faster than hair follicle LRCs in general. From this, we hypothesize that holocrine secretion and turnover of the meibomian gland epithelia is directed from quiescent LRCs located at the junction between ductal and acinar tissue
Because of developmental similarities with skin appendages, and because they both secrete their contents in a holocrine manner, the meibomian gland is considered to be an enlarged, modified sebaceous gland and the mechanism of stem cell renewal is thought to show similar characteristics in these tissues (Knop et al., 2011). Epstein and Epstein (1966) originally showed that skin sebocytes differentiate over two distinct periods, i.e., between 7–9 days and 14–28 days, suggesting that migration and division of cells is heterogeneous in the peripheral basal layer (Epstein and Epstein, 1966), a finding supported by two distinct populations of sebocytes in the human forehead with different labeling indices (Plewig et al., 1971a, Plewig et al., 1971b). Our short-term chase (<16 days) experiments in the H2B-GFP/K5tTA mouse meibomian gland revealed a variation in cell turnover between acini themselves, and between acini and ductal epithelium, suggesting that acini are not in synchrony across a single meibomian gland.
Our data suggest that the region where the duct transitions into an acinus harbors the meibomian gland progenitors, and localized hyperproliferation previously reported in this region (Parfitt et al., 2013) could constitute a transiently amplifying cell population. From this, we propose that LRCs are unipotent, much like the limbal epithelial stem cells that exclusively renew cornea (Amitai-Lange et al., 2015, Collinson et al., 2002, Di Girolamo et al., 2015, Dora et al., 2015), and most likely exist in two populations that separately renew acinar or K6+ ductal tissue.
Sandra Lora Cremers, MD, FACS