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repro bio 3 > Implantation > Flashcards

Implantation Flashcards

1
Q

prior to placental formation, what is early embryo supported by

A
  • secretions of the uterine glands (“uterine milk” or “histotroph”)
  • amino acids, proteins, glucose, ions, growth factors, hormones
  • also directs trophoblast growth and differentiation
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2
Q

importance of histotroph in different species

A
  • superficial placental attachment (pigs, horses, ruminants): important source of nutrition throughout gestation
  • invasive placenta (primates): important for first 1/3 of pregnancy
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3
Q

what is histotroph production under control of

A
  • maternal progesterone and prolactin

- conceptus trophoblast-derived interferons

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4
Q

what does implantation refer to

A

formation of the placenta that will support the embryo and fetus throughout pregnancy

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5
Q

stages of implantation

A
  • apposition
  • adhesion
  • attachment
  • invasion (some species)
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6
Q

is uterine epithelium (endometrium) constantly receptive to implanting embryo

A

no –> there is an “implantation window” where uterus is receptive (“attachment window” in farm species)

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7
Q

what is pre-receptive stage of implantation

A
  • time when embryos of domestic animals grow and become spaced throughout the uterus (cannot adhere)
  • epithelium covered with mucin, MUC-1 (increased by progesterone)
  • these glycoproteins form adhesion barrier
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8
Q

what is the first thing to happen in domestic animal embryo implantation

A

down-regulation or removal of these glycoprotein adhesion barrier molecules to allow apposition of the trophoblast and uterine cells

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9
Q

signals causing down-regulation of glycoprotein adhesion barrier molecules in rodents, farm species

A
  • rodents: increased estrogen
  • farm species: maintained elevated levels of progesterone (down-regulates expression of own receptor, which down-regulates MUC-1 expression)
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10
Q

what happens at the same time as down-regulation of MUC-1

A
  • loss of microvilli
  • further exposure of cell-surface adhesion molecules -production of both uterine epithelial cells and embryonic trophoblast of bridging ligands
  • uterus is now receptive!
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11
Q

other things driving changes to make uterus receptive

A
  • down-regulation of protegesterone receptors

- trophoblast interferons (ruminants - IFN-tau)

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12
Q

what do weak interactions between modified uterine epithelial cells and embryo trigger

A

adhesion cascade, initially using weak interactions between surface carbohydrate molecules (selectins)

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13
Q

what does adhesion cascade do

A

activates or exposes stronger adhesion molecules on the apical surface of the uterine epithelial cells (integrins –> also present on trophoblast cells of embryo)

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14
Q

what do adhesion molecules on trophoblast and epithelial cells do

A
  • each bind to bridging ligands such as fibronectin, vitronectin, osteopontin
  • integrons of embryo attached to these ligands, integrins of uterine epithelium bound to other end –> epithelial structures are bound –> adhesion is stable, embryo attached to uterus
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15
Q

trophoblast in farm species

A
  • does not do much in the way of invasion in to the deeper layers of the uterus
  • pig/horse: no invasiveness –> stays bound to surface of uterine epithelium
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16
Q

what happens if you put pig/horse embryos outside uterus

A
  • aggressively invasive by producing proteolytic enzymes

- uterus secretes protease inhibitors that limit this invasiveness

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17
Q

uterine epithelium of ruminants

A
  • discrete areas (oval) that are devoid of uterine glands –> caruncles
  • between caruncles, epithelium is richly glandular
  • embryonic trophoblast cells overlying carncular epithelium become binucleate, fuse with epithelial cells to form multinucleated syncitial plaques over cauncles
  • embryonic side = cotyledon
  • caruncle + cotyledon = placentome
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18
Q

attachment of embryo, formation of placenta in carnivores, rodents, primates

A
  • blastocyst does gradually invade the uterine stroma
  • once embryo is attached, underlying uterine luminal epithelial cells undergo apoptosis
  • uterine epithelial cells phagocytosed –> endotheliochorial placenta
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19
Q

what does penetration of luminal epithelium by invading trophoblast cells trigger

A
  • responses in the underlying uterine stromal cells termed “decidualization”
  • stromal cells hypertrophy and divide, transforming from small spindle shaped cells to large polygonal cells with extensive contacts between them –> secrete prolactin, IGF binding proteins (control trophoblast invasion)
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20
Q

what is control of cell fusion/invasiveness due to

A

expression of endogenous retroviral sequences present in mammalian genome –> accumulation of these may have had a role in evolution of placenta

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21
Q

what functions does placenta carry out

A
  • functions of lungs, GI tract, kidneys, liver, some endocrine glands
  • steals from mother’s circulation then returns waste products to her for disposal
22
Q

maternal barriers for exchange

A
  • endothelium lining the capillary
  • connective tissue (stroma)
  • uterine epithelium (endometrium)
  • not all layers may be present
23
Q

fetal barriers for exchange

A
  • chorionic epithelium (outermost layer of fetal tissue)
  • connective tissue
  • endothelium lining the capillary
  • all fetal layers present in all cases
24
Q

how are placentas classified

A
  • basis of the maternal-fetal barrier

- outermost maternal later is written first followed by outermost fetal layer (always chorion)

25
Q

what is time of birth (day of gestation) determined by

A

either fetus, the mother, or both (species-dependent)

26
Q

what determines day of birth in sheep

A
  • fetus determines time of birth (maturation of hypothalamo-pituitary-adrenal axis)
  • absence of fetal pituitary gives prolonged gestation
27
Q

what determines day of birth in rabbits, rodents, marsupials

A
  • maternal control

- fetal decapitation has little or no effect on time of birth

28
Q

what determines day of birth in primates

A

both fetal and maternal factors

29
Q

progesterone effects on uterine contractility

A
  • important in maintaining the absence of uterine contractions (uterine quiescence)
  • prevents formation of estrogen receptors, prevents gap junction formation between myometrial cells, reduces uterine innervation so b-adrenergic influences (relaxant) predominate, prevents oxytocin/prostaglandin receptor formation, prevents action of relaxin to soften cervix
30
Q

estrogen effects on uterine contractility

A
  • promotes uterine contractility
  • induces receptors for uterotonic agents (oxytocin, a-adrenergics, prostaglandins), induces receptors for uterine relaxants (b-adrenergics), induces gap junctions between myometrial cells (promotes coordination/propagation of contractions), promotes synthesis of prostaglandins in animals with previous progesterone exposure
31
Q

prostaglandin effects in late pregnancy/parturition

A
  • luteolysis and synergize with oxytocin in promoting uterine contraction
  • stimulation of uterine contraction, remodeling cervix prior to birth
  • formation stimulated by oxytocin
32
Q

relaxin effects in late pregnancy

A
  • rat/pig/human: primary source is CL (released in association with luteal regression)
  • cat/dog/horse/rabbit: primary source is placenta (release can be at any time)
  • receptors in cervix, uterus, mammary gland, etc
  • acts on CT in cervix, pelvic ligaments to cause softening and relaxation
33
Q

3 ways oxytocin acts in late pregnancy

A
  • causes myometrial contractions
  • causes release of PGF2a from uterine endometrium
  • causes release of PGE2 from mucosa of cervix
34
Q

oxytocin increases in late pregnancy

A
  • increase in receptor number occurs near term to increase tissue responsiveness
  • increased expression of receptors due to increase in estradiol/progesterone (E/P) ratio
  • rabbits/rodents/carnivores: due to decline in progesterone level, increase in estrogen
  • other species: progesterone levels remain high - increase in estrogen alone changes E/P ratio
35
Q

oxytocin and CNS in late pregnancy

A
  • synthesis increases, nesting behavior is exhibited
  • approaching term, circadian rhythm in uterine contractions is established - increases in nocturnal activity
  • contractions are in response to oxytocin release
36
Q

sheep and progesterone

A

production from ~day 60 is placental - CL no longer required

37
Q

what causes birth in sheep

A
  • maturation of the fetal hypothalamo-pituitary-adrenal axis
  • hypophysectomy (removes ACTC) or disconnect of the hypothalamus and pituitary gland prevents partutition
  • same in fetuses that are anencephalic
38
Q

sheep placenta and hormones

A
  • secretes progesterone
  • for most of pregnancy cannot make estrogens because it backs sufficient activity of 17a-hydroxylase enzyme (can’t convert progestagens into androgens)
39
Q

sheep fetal adrenals

A
  • mature in last week of pregnancy
  • respond to ACTH from fetal pituitary by producing cortisol
  • increase in pituitary ACTH secretion and increase in sensitivity of the adrenals to this stimulus
40
Q

“new story” (extra step) in sheep parturition

A

-increased cortisol increases prostaglandin synthase II (cox-2) in placental trophoblast (fetal), which increases PGE2 production

41
Q

initial actions of PGE2 in sheep partutition (2)

A
  • placental PGE2 acts in autocrine/paracrine manner to increased P450c17 enzyme (17a-hydrozylase), which allows conversion of pregnenolone to androgens –> estrogen (surge in placental estrogen)
  • placental PGE2 has positive feedback on fetal hypothalmo-pituitary-adrenal axis to sustain the increase in fetal cortisol output
42
Q

functions of increases in estrogen/progesterone ratio in sheep (4) and ultimate purpose

A
  • increases oxytocin pulses from posterior pituitary
  • increases oxytocin receptors on the endometrium, myometrium, other tissues
  • increases formation of gap junctions in the myometrium (smooth muscles more coordinated)
  • increases PGF2a formation in maternal endometrial tissue
  • purpose: increase uterine contractions
43
Q

what does increased PGF2a secretion do around parturition (2)

A
  • causes luteolysis (of remaining CL functionality)

- causes release of relaxin from CL that aids PGE2 in softening of the cervix and pelvic ligaments

44
Q

what happens to oxytocin during partutition

A
  • ferguson’s reflex induces surge of oxytocin that causes powerful uterine contractions
  • these and muscle contractions of abdominal wall deliver the fetus
  • prostaglandin synergizes with oxytocin to increase force of myometrial contractions
45
Q

hypoglycemia and maturation of fetal hypothalamo-pituitary-adrenal axis

A
  • fetus is normally hypoglycemic in relation to the mother to allow glucose transfer down concentration gradient
  • fetal pituitary responds to hypoglycemia by increasing ACTH secretion –> becomes more sensitive to hypoglycemia
  • may activate HPA axis and cause large cortisol increases that induce parturition
46
Q

leptin and maturation of fetal hypothalamo-pituitary-adrenal axis

A

energy stress in late pregnancy leads to fetal fat catabolism –> decreased adipose stores –> decreased leptin –> increased neuropeptie Y –> activation of HPA axis –> increased CRH and AVP –> birth cascade

47
Q

cows/goats and initiation of birth cascade

A
  • progesterone maintaining pregnancy is from CL (20% from placenta)
  • maturation of fetal adrenal axis and secretion of cortisol induces enzymes that convert this placental progesterone into estrogen
  • causes production of endometrial PGF2a and birth cascade
48
Q

dogs/cats and initiation of birth cascade

A
  • progesterone is from multiple CLs throughout pregnancy in bitch, some from placenta in queen
  • trigger for parturition unknown
  • some fetal involvement?
49
Q

primates and progesterone near the end of pregnancy

A
  • no reduction in progesterone prior to labor
  • effective estrogen/progesterone ratio still needs to be altered in favor of estrogen if uterine contractile mechanisms are to work
50
Q

how is estrogen/progesterone ratio altered in primates (3)

A
  • placenta lacks 17a-hydroxylase –> cannot form androgens to produce estrogen - however, enzyme is not inducible by cortisol - fetal adrenal has “fetal zone” that synthesizes androgens in response to ACTH –> move to placenta, converted to estrogens
  • “functional progesterone withdrawal”
  • cortisol antagonizes many progesterone actions - high levels of cortisol in placenta mean that progesterone functions are reduced within the uterus –> shift in local E:P ratio
51
Q

what do changes in E:P ratio do in primates

A
  • increase oxytocin receptors, myometrial gap junctions, and prostaglandin synehtsis
  • have oxytocin production locally within the uterus too
52
Q

circadian timing of parturition

A
  • many species give birth at set time of day
  • function of circadian clock
  • action of maternal clock sets fetal clock

repro bio 3 (6 decks)

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