Proof that Growth Factors are Needed for Meibomian Gland Health

In my research into the potential benefit of Stem Cell Injections into the Meibomian Gland, I wondered if there has been proof that Meibomian Glands need Growth Factors to grow. While it seems intuitive that they do, I wondered what the literature said about Meibomian Glands and Growth Factors. This article in a well respected journal demonstrates the need for Fibroblast Growth Factor Receptors for Meibomian Gland health, at least in adult mice.

Stromal vascular fraction (SVF), which is the product you get by isolating stem cells from fat tissue contains multiple Growth Factors. This is just another example of why SVF should regenerate Meibomian Glands.

Invest Ophthalmol Vis Sci. 2017 May 1;58(5):2638-2646. doi: 10.1167/iovs.16-21204.

Fibroblast Growth Factor Receptor 2 (FGFR2) Is Required for Meibomian Gland Homeostasis in the Adult Mouse.

Reneker LW1, Wang L1, Irlmeier RT1, Huang AJW2.

Author information

Abstract

PURPOSE:

Little is known about the signaling mechanisms controlling meibomian gland (MG) homeostasis and the pathogenic processes leading to MG atrophy and dysfunction in dry eye disease (DED). We investigated the role of fibroblast growth factor receptor 2 (FGFR2) in the MG homeostasis of adult mice.

METHODS:

A triple transgenic mouse strain (Krt14-rtTA; tetO-Cre; Fgfr2flox/flox), referred to as Fgfr2CKO mice, was generated in which the Fgfr2 gene is ablated by Cre recombinase in keratin 14 (Krt14)-expressing epithelial cells on doxycycline (Dox) induction. FGFR2 expression in normal human and mouse MGs was evaluated by immunohistochemistry. Pathologic MG changes in transgenic mice with conditional deletion of FGFR2 were examined by lipid staining, histology, and immunostaining.

RESULTS:

FGFR2 was highly expressed in normal human MGs and adult mouse MGs. Two-month-old Fgfr2CKO mice fed Dox-containing chow for 2 weeks developed severe MG atrophy. MG acinar atrophy in the Fgfr2CKO mice was associated with reduced lipid (meibum) production and the development of clinical findings similar to those in humans with evaporative DED related to MG dysfunction (MGD). Immunohistochemical analyses showed that FGFR2 deletion severely affected proliferation and differentiation of MG acinar cells but affected MG ductal cells to a lesser extent.

CONCLUSIONS:

FGFR2 deletion results in significant MG acinar atrophy and clinical manifestations of MGD in Fgfr2CKO mice, suggesting that MG homeostasis is FGFR2 dependent. The Fgfr2CKO mice with inducible MG atrophy can serve as a valuable animal model for investigating the pathogenesis of MGD and developing novel therapeutic strategies for MGD-related DED.