Page 63
allied
academies
Cell Science, Stem Cell Research &
Pharmacological Regenerative Medicine
November 29-30, 2017 | Atlanta, USA
Annual Congress on
Adv cel sci tissue cul 2017 | Volume 1 Issue 2
T
he discovery of the gap junction structure, its functions and
the family of the connexin genes, has been basically ignored
by the major biological disciplines. These connexin genes code
for proteins that organize to form membrane-associated hemi-
channels, connexons, co-joinwith the connexons of neighboring
cells to form gap junctions. Gap junctions appeared in the early
evolution of the metazoan. Their fundamental functions, (e.g.,
to synchronize electrotonic andmetabolic functions of societies
of cells and to regulate cell proliferation, cell differentiation and
apoptosis), were accomplished via integrating the extra-cellular
triggering of intra-cellular signaling and therefore, regulating
gene expression. These functions have been documented
by genetic mutations of the connexin genes and by chemical
modulation of gap junctions. Via genetic alteration of connexins
in knock-out and transgenic mice, as well as inherited connexin
mutations in various human syndromes, the gap junction has
been shown to be directly linked to many normal cell functions
and multiple diseases, such as birth defects, reproductive,
neurological disorders, immune dysfunction and cancer.
Specifically, the modulation of gap junctional intercellular
communication (GJIC), either by increasing or decreasing
its functions by non-mutagenic chemicals or by oncogenes
or tumor suppressor genes in normal or initiated stem cells
and their progenitor cells, can have a major impact on tumor
promotion or cancer chemoprevention and chemotherapy. The
overview of the roles of the gap junction in the evolution of
the metazoan and its potential in understanding a system view
of human health and aging and the diseases of aging will be
attempted.
e:
James.Trosko@hc.msu.eduThe gap junction as a biological rosetta stone: Implications of evolution stem cells to homeostatic regulation
of health and disease in the barker hypothesis
James E Trosko
Michigan State University, USA