Impaired microcirculation can cause lymphatic leakage which leads to a chronic swelling in the tissues of the body. However, no successful treatment gives any protection against
lymphedema due to the lack of well-revealed pathophysiology of secondary
lymphedema. Binary image of
laminin immunohistochemical expression revealed that distribution of
laminin expression localized during surgically induced
lymphedema. 67 kDa
laminin receptor (67LR)
mRNA expression showed a peak at during
lymphedema exacerbation. Since the response of 67LR molecules may affect the prevention of
inflammation and
edema, here we have hypothesized that 67LR
ligand of
YIGSR peptide could permit reconstructive environment for amelioration of
lymphedema and evaluated the effect of
YIGSR in a mouse tail model of
lymphedema. Indeed, intra-abdominal
injections of
YIGSR for the first 3 days after inducing
lymphedema in the mouse tail model reduced the tail
lymphedema on day 14 by 27% (P = 0.035). Histology showed that
YIGSR treatment protected
lymphedema impairment in epidermis and dermis, and it also inhibited the expansion of intercellular spaces and enhanced especially cell adhesion in the basement membrane as revealed by transmission electron microscopy. Interestingly, the treatment also reduced the local expression of
transforming growth factor (TGF)β. Further elucidation of the mechanisms of 67LR-facilitated lymphangiogenesis contributes to find potential targets for the treatment of
lymphedema.