Fixing Birthweight Reduction Problems

In Normal pregnancy, the uteroplacental arteries are invaded by endovascular trophoblast and
remodeled into dilated, inelastic tubes without maternal vasomotor
control. (https://academic.oup.com/biolreprod/article/69/1/1/2712724) However, in
Preeclampsia, the disease results from defective spiralartery remodelling, leading to cellular
ischaemia in the placenta, which in turn results in an imbalance between anti-angiogenic and
pro-angiogenic factors. This imbalance in favour of anti-angiogenic factors leads to
widespread endothelial dysfunction, affecting all the maternal organ systems. In addition,
there is foetal growth restriction (FGR). (https://www.ncbi.nlm.nih.gov/pubmed/27213853).

Failure of invasive trophoblasts to penetrate and convert the maternal spiral arterioles/arteries
causes poor uteroplacental perfusion.This leads to a vicious cycle of cellular ischemia and
hypoxia, oxidative stress, vascular endothelial injury, and the release of inflammatory factors,
which eventually lead to maternal and fetal clinical symptoms.
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753693).

Researcher founds that Mesenchymal stem cells (MSCs) are self-renewal and multipotent,
and, in addition, MSCs secrete a great variety of cytokines, have immunosuppressive
abilities, and are not very immunogenic. In addition, Human umbilical cord is most often
treated as medical waste and is abundantly available. Compared with MSCs from other
sources, human umbilical cord MSCs (hUCMSCs) have an excellent proliferation rate, a
greater expansion potential, and a strong immunosuppressive capability and can be easily and
noninvasively obtained from Wharton's jelly without ethical constraints, and hUCMSCs also
can differentiate into osteocytes, adipocytes, chondrocytes, endothelial cells, and so on. It is
also found that hUCMSCs can regulate trophoblast cell functions. When trophoblast cells are
treated with hUCMSC supernatant or cocultured them with hUCMSCs, both treatments
remarkably enhanced the migration and invasion abilities of trophoblast cells and upregulated
their proliferation ability. At a certain concentration, hUCMSCs also modulated hCG, PIGF,
and Endoglin levels in the trophoblast culture medium. Thus, hUCMSCs have a positive
effect on trophoblast cellular functions.
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753693/). This can leads to fetal weight
gains on pre-eclampsia.

Fixing Renal Impairment

In normal pregnancy, glomerular filtration rate (GFR) as measured by inulin clearance and
renal plasma flow (para-aminohippurate clearance) increases by 40% to 60% during the first
trimester. This results in a fall in serum markers of renal clearance, including blood urea
nitrogen (BUN), creatinine, and uric acid. In preeclampsia, both GFR and renal plasma flow
decrease by 30% to 40% compared with normal pregnancy of the same duration.
(http://www.sciencedirect.com/science/article/pii/S0085253815506996#bb0385).
Several mechanisms might explain the observed association between preeclampsia and
subsequent renal disease. One possibility is that kidney disease and preeclampsia are caused
by the same factors. Obesity, hypertension, insulin resistance, and endothelial dysfunction,
for example, have been linked to both disorders.Antiangiogenic factors have been suggested
to have an important role in the pathogenesis of preeclampsia and in the progression of
chronic renal disorders. Alternatively, preeclampsia may exacerbate subclinical kidney
disease that is present before pregnancy. This hypothesis is consistent with previous finding
that preeclampsia was associated with similar relative risks for receiving a diagnosis of a
specific type of renal disease on renal biopsy and for undergoing a renal biopsy. The
hypothesis is also consistent with present finding that preeclampsia is associated with similar
relative risks for the development of End-Stage Renal Disease (ESRD) due to a specific cause
and for the development of ESRD in general. A third possibility is that preeclampsia may
cause later renal disease. The observation in other studies that 20 to 40% of women with
preeclampsia have microalbuminuria 3 to 5 years after pregnancy, as compared with only 2%
of women without preeclampsia.
(http://www.nejm.org/doi/full/10.1056/NEJMoa0706790#t=article)
The HUC-MSCs improved kidney injury induced by I/R as demonstrated by enhancement of
the kidney function via decreasing serum levels of creatinine, urea and uric acid. The
therapeutic efficacy of HUC-MSCs were found to be mediated through anti-oxidant activity
as indicated by significant reduction in total malondialdehyde (MDA) and significant
increment in the levels of reduced glutathione (GSH), catalase (CAT) and glutathione-S-
transferase (GST). The present work suggests that HUC-MSCs may be an effective
therapeutic agent against renal IRI. The recorded data showed improvement of renal
functions and urine albumin in HUC-MSCs than IRI group with positive antioxidant efficacy
of HUC-MSCs through scavenging free radicals and supporting the antioxidant enzymes.
(https://www.ncbi.nlm.nih.gov/pubmed/28476205).