The role of forskolin as a lipolytic stimulator during in vitro oocyte maturation and the in vitro embryo production of livestock

Abstract

Cryopreservation is a modern technique which assists in the preservation of genetic material from oocytes and embryos for a long time. However, elevated vulnerability to cryopreservation due to the large accumulation of intracellular lipids within oocytes or embryos avoids success of this method. These lipids remain the main crucial factor limiting survival rates of oocytes and embryos after thawing. Lipid ingathering in the oocyte cytoplasm augments lipid peroxidation (LPO) and oxidative stress increases the apoptosis process, declines the viability after thawing, declines cytoskeleton actin filament injuries, lowers the blastocyst rates and reduces cryotolerance in the early stages of embryo development. There have been several attempts to reduce the ingathering of intracellular lipids in oocytes or embryos during the cryopreservation process, in that way enhancing the competence of cryopreserved oocytes or embryos and increasing their viability. One of the most applied agents for chemical delipidation is forskolin. Forskolin exhibited a possible part in improving the oocytes cryopreservation through stimulating cyclic adenosine monophosphate (cAMP) production. The main purpose of cAMP modulation is to provide energy to sustain the mammalian oocytes´ meiotic arrest. The purpose of the existing article is to assess and offer more evidence concerning the forskolin utilization as a modulator of cAMP during the cryopreservation of oocytes and its influence on meiosis completion and the reorganization of cytoplasm, which are prerequisites for the development of oocytes in addition to the contribution to fertilization and subsequently, the development of embryos.

The combination of rolipram and cilostamide improved the developmental competence of cloned porcine embryos

“…Similarly, cilostamide inhibited the activity of PDE3A in rodents and macaque oocytes 65 , 66 . Forskolin, another PDE3A inhibitor, successfully regulated cAMP in mouse 67 , 68 , rat 69 , 70 , dog 71 , and pig 72 oocytes.…”

“…Similarly, cilostamide inhibited the activity of PDE3A in rodents and macaque oocytes 65,66 . Forskolin, another PDE3A inhibitor, successfully regulated cAMP in mouse 67,68 , rat 69,70 , dog 71 , and pig 72 oocytes.Despite progressive efforts, the in vitro competence of oocytes remains lower than that of their in vivo counterparts. On the other hand, rolipram as PDE4 inhibitor has showed a delaying effect on the spontaneous meiotic maturation during in vitro maturation through extended gap junctional communication between CCs and the oocyte, and subsequently improved cytoplasmic maturation and developmental potential of oocyte 73 .…”

The Adenylyl Cyclase Activator Forskolin Increases Influenza Virus Propagation in MDCK Cells by Regulating ERK1/2 Activity

“…AC catalyzes the conversion of adenosine triphosphate to 3',5'-cyclic adenosine monophosphate (cAMP) [ 11 ], which is involved in a wide range of cellular processes (including cell proliferation, apoptosis, immune response, and neurohormonal signaling) as a second messenger [ 12 , 13 ]. Intracellular cAMP levels can be elevated by various agents including forskolin (FSK), prostaglandin E2 (PGE2), and 3-isobutyl-1-methylxanthine (IBMX) [ 14 , 15 ].…”