Evidence map›Paper›PMID 21123735›Full record

ArticleAmerican journal of physiology. Cell physiology2011

Soluble adenylyl cyclase mediates bicarbonate-dependent corneal endothelial cell protection.

Shimin Li, Kah Tan Allen, Joseph A Bonanno

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Pharmacological modulation of the COPharmacology & therapeutics · 2018
    Review
  3. Article
  4. Article
  5. Soluble adenylyl cyclase in health and disease.Biochimica et biophysica acta · 2014
    Review
  6. Article
  7. Soluble adenylyl cyclase in the eye.Biochimica et biophysica acta · 2014
    Review
  8. Review
  9. Review
  10. Soluble adenylyl cyclase activity is necessary for retinal ganglion cell survival and axon growth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  11. Role of soluble adenylyl cyclase in the heart.American journal of physiology. Heart and circulatory physiology · 2012
    Review
  12. Review
  13. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Shimin LiSchool of Optometry, Indiana University, 800 E. Atwater Ave., Bloomington, IN 47405, USA.
Kah Tan Allen
Joseph A Bonanno
Indiana University Bloomington · US

Funding

REGULATION OF PHI AND FLUID FLUX IN CORNEAL ENDOTHELIUMR01EY008834 · NEI · UNIVERSITY OF CALIFORNIA BERKELEY · PI BONANNO, JOSEPH AURELIO · 1991 to 2020
$7.8M
Core Support for Vision Research at Indiana UniversityP30EY019008 · NEI · TRUSTEES OF INDIANA UNIVERSITY · PI BURNS, STEPHEN A · 2009 to 2013
$2.1M
NEI NIH HHS EY08834NEI NIH HHS P30 EY019008NEI NIH HHS R01 EY008834
6 · The paper itself

Abstract

Cyclic AMP produced from membrane receptor complex bound adenylyl cyclases is protective in corneal endothelial cells (CEC). CEC also express soluble adenylyl cyclase (sAC), which is localized throughout the cytoplasm. When activated by HCO(3)(-), cAMP concentration ([cAMP]) increases by ∼50%. Here we ask if cAMP produced from sAC is also protective. We examined the effects of HCO(3)(-), pH, phosphodiesterase 4 inhibition by rolipram, sAC inhibition by 2HE (2-hydroxyestradiol), and sAC small interfering RNA (siRNA) knockdown on basal and staurosporine-mediated apoptosis. HCO(3)(-) (40 mM) or 50 μM rolipram raised [cAMP] to similar levels and protected endothelial cells by 50% relative to a HCO(3)(-)-free control, whereas 2HE, which decreased [cAMP] by 40%, and H89 (PKA inhibitor) doubled the apoptotic rate. sAC expression was reduced by two-thirds in the absence of HCO(3)(-) and was reduced to 15% of control by sAC siRNA. Protection by HCO(3)(-) was eliminated in siRNA-treated cells. Similarly, caspase-3 activity and cytochrome c release were reduced by HCO(3)(-) and enhanced by 2HE or siRNA. Analysis of percent annexin V+ cells as a function of [cAMP] revealed an inverse, nonlinear relation, suggesting a protective threshold [cAMP] of 10 pmol/mg protein. Relative levels of phosphorylated cAMP response element binding protein and phosphorylated Bcl-2 were decreased in CEC treated with 2HE or siRNA, suggesting that HCO(3)(-)-dependent endogenous sAC activity can mobilize antiapoptotic signal transduction. Overall, our data suggest a new role for sAC in endogenous cellular protection.

Indexed as

Adenylyl Cyclase InhibitorsAdenylyl CyclasesAnimalsAnnexin A5ApoptosisBicarbonatesCaspase 3CattleCells, CulturedCyclic AMPCyclic AMP Response Element-Binding ProteinCytochromes cEpithelium, CornealEstradiolIsoquinolinesPhosphodiesterase 4 Inhibitors2-hydroxyestradiolAdenylyl Cyclase InhibitorsAdenylyl CyclasesAnnexin A5BicarbonatesCaspase 3Cyclic AMPCyclic AMP Response Element-Binding ProteinCytochromes cEstradiolIsoquinolinesN-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamidePhosphodiesterase 4 InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-bcl-2RNA, Small InterferingRolipramStaurosporineSulfonamides

Identifiers

PMID21123735
PMCPMC3043628
OpenAlexW2059300616

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.