Activated caspace-3 staining of mouse cardiac sections showing apoptosis in sham, 8 weeks post-AB (AB 8 wks) treated with vehicle control and Mdivi.

<p><b>A</b>) Apoptotic cells are seen as red fluorescent dots (scale bar- 20 µm). <b>C</b>) Activated caspace-3 +ve cells represented in an enlarged area. <b>B</b>) Data represents mean ±SE from n = 6 per group; *p<0.05 was considered significant compared to sham and ^#p<0.05 compared to vehicle treated group.</p

IHC staining of mouse heart sections with mitochondrial marker antibody MTCO-2 in sham, 8 weeks post-AB (AB 8 wks) treated with vehicle control and Mdivi.

<p><b>A</b>) Expression of MTCO-2 is seen as red fluorescence intensity (scale bar-50 µm). <b>B</b>) Data represents mean ±SE from n = 6 per group; *p<0.05 was considered significant compared to sham and ^#p<0.05 compared to vehicle treated group.</p

Tunnel assay of mouse cardiac sections staining for apoptosis in sham, 8 weeks post-AB (AB 8 wks) treated with vehicle control and Mdivi.

<p><b>A</b>) Apoptotic cells are seen as green fluorescent dots (scale bar- 10 µm). Positive and negative controls are also represented in this image. <b>B</b>) Data represents mean ±SE from n = 6 per group; *p<0.05 was considered significant compared to sham and ^#p<0.05 compared to vehicle treated group.</p

Mdivi promotes angiogenesis.

<p><b>A</b>) CD-31-immunohistochemical (IHC) staining of heart and secondarily stained with alexaflour 647 in sham, 8 weeks post-AB (AB 8 wks) treated with vehicle control and Mdivi. The expression of CD31 is seen as red fluorescence intensity (scale bar- 20 µm). <b>C</b>) VEGF-IHC staining of heart sections, secondarily stained with alexaflour 594 in sham, 8 weeks post-AB (AB 8 wks) treated with vehicle control and Mdivi. The expression of VEGF is seen as red fluorescence intensity (scale bar- 50 µm). <b>B, D</b>) Data represents mean ±SE from n = 6 per group; *p<0.05 compared to sham and ^#p<0.05 compared to vehicle treated group.</p

mRNA expression of endostatin and angiostatin primers.

<p><b>A</b>) RT-PCR: mRNAs are amplified using respective primers and the bands were quantified using densitometry. <b>B, C</b>) Bar graphs represent respective mRNA expression over GAPDH expression by RT-PCR and real time PCR assay. Data represents mean ±SE from n = 6 per group; *p<0.05 was considered significant compared to sham and ^#p<0.05 compared to vehicle treated group.</p

IHC staining of heart sections with mitophagy markers LC3 and P62 in sham, 8 weeks post-AB (AB 8 wks) treated with vehicle control and Mdivi.

<p><b>A</b>) Expression of LC3 is seen as green fluorescence intensity and P62 as red fluorescence intensity (scale bar- 10 µm). <b>B</b>) Data represents mean ±SE from n = 6 per group; *p<0.05 was considered significant compared to sham and ^#p<0.05 compared to vehicle treated group.</p

mRNA primers.

<p>mRNA primers.</p

mRNA expression of MMP-9 and TIMP-3.

<p>A) mRNAs are amplified using respective primers and the bands were quantified using densitometry. <b>B, C</b>) Bar graphs represent respective mRNA expression over GAPDH expression by RT-PCR and real time PCR assay. Data represents mean ±SE from n = 6 per group; *p<0.05 was considered significant compared to sham and ^#p<0.05 compared to vehicle treated group.</p

Mdivi ameliorates left ventricular dysfunction.

<p><b>A</b>) Changes in left ventricular (LV) function following aortic banding (AB) and the effects of Mdivi treatment, a Drp1 inhibitor. Representative M-mode echocardiography images from sham, sham with Mdivi treatment, AB 8 weeks with vehicle and Mdivi treatment groups. The bar graphs represent LVIDd (left ventricular internal dimension in diastole), LVPWd (left ventricular posterior wall dimension in diastole (<b>B</b>), and %FS (percentage fractional shortening) (<b>C</b>). *p<0.05 compared to sham and ^#p<0.05 compared to vehicle treated group. Data represents mean ±SE from n = 6 per group.</p

Metabolic engineering of <i>Escherichia coli</i> W3110 strain by incorporating genome-level modifications and synthetic plasmid modules to enhance L-Dopa production from glycerol

<p>L-Tyrosine which is one of the terminal metabolites of highly regulated aromatic amino-acid biosynthesis pathway in <i>Escherichia coli</i> is a precursor for synthesis of L-Dopa. In this study, we report over production of L-Dopa by enhancing expression of rate limiting isoenzyme of shikimate kinase (aroL), chorismate synthase (aroC), aromatic-amino-acid aminotransferase (tyrB) and 3-phosphoshikimate 1-carboxyvinyltransferase (aroA) form a plasmid module harboring five enzymes under two inducible promoters converting shikimate to tyrosine. 4-hydroxyphenylacetate-3-hydrolase (hpaBC) which converts L-Tyrosine to L-Dopa was expressed constitutively from a separate plasmid module. Feedback deregulated expression of 3-Deoxy-D-arabinoheptulosonate-7-phosphate (DAHP) synthase (aroG*) replacing wild type aroG under its natural promoter led to enhancement of L-Dopa production. Deletion of transcriptional repressor tyrR and links to other competing pathways improved titers of L-Dopa. We focused on having a balanced flux by constitutive expression of pathway enzymes from plasmid constructs rather than achieving higher amounts of catalytic protein by induction. We observed glycerol when used as a carbon source for the final strain led to low acid production. The best performing strain led to decoupling of acid production and product formation in bioreactor. Fed batch analysis of the final strain led to 12.5 g/L of L-Dopa produced in bioreactor.</p