PowerPoint 5 Notes

Steroid Receptors and Second Messenger System

 

1)      Steroid Second Messenger  - Power Point Figure

a)      Using Estrogen as an example:  Estrogen in the blood combines with sex binding protein (SBP) that makes the molecule bigger.

b)      Steroid hormones bind to receptors in the nucleus as opposed to protein hormones that bind to receptors in the plasma membrane.

c)      The estrogen binds to its receptor in the nucleus. This unit of hormone + receptor is referred to as the transcription factor.

d)      This transcription factor attaches to DNA in the nucleus leading to synthesis of RNA.

e)      After transcription the RNA is moved out of the nucleus to the rough endoplasmic reticulum where it is made into proteins through translation.

 

Note: All hormones induce their own receptors.

 

2)      Estrogen and Progesterone Binding to Receptors Alters Cell Function.

a)      Estrogen-Proliferative.

i)        Estrus-high levels E2 induces behavioral estrus.

ii)       Prior to ovulation-releases preovulatory surge of LH.

iii)     Prepares cervix, uterus & oviduct for sperm egg transport, fertilization and migration of fertilized egg.

iv)     Induces P4R.

v)      Induces E2R.

(1)   Increases mRNA.

(2)   Increases blood flow.

(3)   Increases H20 uptake.

(4)   Increases cell expansion.

(5)   Increases cell growth.

(6)   Increases OTR.

(7)   Closes epiphyseal plates in male and female.

 

b)      Progesterone-Secretory.

i)        P4 from CL.

ii)       Inhibits ovulation (LH, GnRH) surge.

iii)     Prepares uterus and cervix for pregnancy & implantation.

(1)   Inhibits E2R.

(2)   Induces P4R

(3)   Inhibits P4R after about day 12 of the estrous cycle, down regulating its own receptor.

 

Note: P4 has long been considered an antagonist of estrogen action. The delicate balance and interactions between these ovarian hormones are essential for many reproductive functions. P4 decreases the ability of the uterus to respond in a totally estrogen-directed fashion. P4 reduces and or redirects the ability of the uterine cells to respond to E2. This interaction produces an appropriate uterine environment for pregnancy.